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Am J Hum Genet. 2003 Jan; 72(1): 125–131.
Published online 2002 Dec 9. doi:  10.1086/345646
PMCID: PMC378616

A Susceptibility Gene for Psoriatic Arthritis Maps to Chromosome 16q: Evidence for Imprinting


Several genetic loci have been reported for psoriasis, but none has been specifically linked to psoriatic arthritis (PsA), a condition that affects >10% of patients with psoriasis. A genetic component for PsA is suggested by segregation within families and high concordance among identical twins. We performed a linkage scan to map genes contributing to PsA. We identified 178 patients with PsA out of 906 patients who were included in our genetic study of psoriasis. Using a comprehensive genealogy database, we were able to connect 100 of these into 39 families. We genotyped the patients using a framework marker set of 1,000 microsatellite markers, with an average density of 3 cM, and performed multipoint, affected-only, allele-sharing linkage analysis using the Allegro program. On the basis of the initial results, we genotyped more markers for the most prominent loci. A linkage with a LOD score of 2.17 was observed on chromosome 16q. The linkage analysis, conditioned on paternal transmission to affected individuals, gave a LOD score of 4.19, whereas a LOD score of only 1.03 was observed when conditioned for maternal transmission. A suggestive locus on chromosome 16q has previously been implicated in psoriasis. Our data indicate that a gene at this locus may be involved in paternal transmission of PsA.


Psoriasis (MIM 177900) is a common inflammatory skin disease that may have an autoimmune basis and be predominantly mediated by T lymphocytes (Baker et al. 1984; Valdimarsson et al. 1995; Prinz 1999). Several overlapping clinical types of the disease have been identified, but the chronic plaque form (psoriasis vulgaris) is most common and is characterized by well-demarcated, indurated, erythematous, and scaly lesions, or plaques, most frequently located on knees, elbows, or scalp. The lesions are infiltrated by inflammatory cells, but a marked increase in proliferation and turnover of keratinocytes distinguish psoriasis from other inflammatory skin diseases. The disease has a strong but complex genetic basis, with a concordance rate of 50%–70% among MZ twins (Farber et al. 1974; Eastmond 1994; Costello and FitzGerald 2001). Several genetic loci have been suggested, but only a major histocompatability (MHC) locus on chromosome 6 has been independently reported by at least two groups as significant genomewide (Elder et al. 2001). Psoriasis has a strong association with the Cw6 allele of the HLA-C gene in the MHC (Tiilikainen et al. 1980). Accordingly, strong linkage to the MHC region on chromosome 6p has been observed in most populations studied (Trembath et al. 1997; Jenisch et al. 1998; Samuelsson et al. 1999) and has been localized to the vicinity of HLA-C by linkage disequilibrium mapping (Balendran et al. 1999; Oka et al. 1999; Nair et al. 2000). Psoriatic arthritis (PsA) has been recognized since the late 19th century (Moll and Wright 1973a; Fearon and Veale 2001; Patel et al. 2001). It affects >10% of patients with psoriasis (Gladman et al. 2001), and, in most cases, there is an association between the severity of the arthritis and the skin involvement (Winchester 1995).

Several types of characteristic nail lesions are observed in 35%–40% of patients with psoriasis, including pitting, onycholysis, subungual hyperkeratosis, and dystrophy, and it has been reported that PsA is more common in patients with nail changes (Rahman et al. 2000). Several different types of PsA have been identified, and, in contrast to rheumatoid arthritis, most patients with PsA are negative for rheumatoid factor (Moll and Wright 1973a). Although a clear genetic component has been reported in PsA, with a concordance rate range of 30%–70% among MZ twins (Moll and Wright 1973b; Winchester 1995), there is, to our knowledge, no report of a genetic locus for the arthritic manifestations of psoriasis. We have recently found that PsA is somewhat more common in patients with HLA-Cw6 negative than those with Cw6 positive (Gudjonsson et al. 2002). We find that psoriatic nail lesions are also observed more often in patients with PsA. Several association studies dealing with the genetics of PsA that focused on the MHC (Bruce and Silman 2001; Gladman et al. 2001; Gonzalez et al. 2001, 2002; Al-Heresh et al. 2002) found greater excess of one allele or another over the Cw6 allele associated with skin psoriasis. The association to the MHC is present in PsA, although it is less pronounced than in the skin manifestations (Eastmond 1994; Gonzalez et al. 2002). The only other study to attempt linkage analysis on families with PsA was performed in a Scottish population, typing 11 microsatellite markers at three psoriasis loci described elsewhere (Burden et al. 1998). Although a significant LOD score was obtained for psoriasis, no evidence of linkage was detected for PsA. A recent epidemiological study has indicated that there are more patients suffering from PsA who have affected fathers than have affected mothers (Rahman et al. 1999). In the course of performing linkage analysis on families with psoriasis, we observed a locus on chromosome 16q, with linkage to PsA, that exhibited an even higher LOD score when the study was restricted to pairs of affected relatives in whom the last transmission came from the father.

Subjects and Methods

This study was approved by the National Bioethics Committee of Iceland and the Data Protection Committee of Iceland. Informed consent was obtained from all individuals whose DNA was used in our analysis. We used our comprehensive Icelandic genealogical database (Gulcher and Stefansson 1998) to automatically create families that included patients separated up to and including seven meioses (six meioses separate second cousins). All personal identifiers associated with medical information and blood samples were reversibly encrypted by the Data Protection Committee of Iceland (Gulcher et al. 2000). The Icelandic genealogical database was also encrypted by the Data Protection Committee of Iceland (Gulcher et al. 2000).

Of 906 patients with chronic plaque psoriasis whom we have evaluated clinically, 178 patients had been diagnosed with and treated for PsA by rheumatologists. The diagnostic criteria were inflammatory arthritis, seronegativity for rheumatoid factor, and unequivocal psoriatic skin lesions at the time of diagnosis of PsA. We genotyped these patients using a 1,000-marker fluorescent labeled microsatellite screening set with an average density of 3 cM in the genome, where genetic locations are based on the Decode map (Kong et al. 2002). Additional markers were genotyped for the regions showing the strongest evidence for linkage, increasing the density up to ∼1 cM. Genotyping was performed with our standard conditions (Gretarsdottir et al. 2002).

All reported LOD scores were calculated with Allegro (Gudbjartsson et al. 2000). The program computes nonparametric, multipoint, affected-only, and allele-sharing LOD scores on the basis of the S-pairs scoring function (Kruglyak et al. 1996) and an exponential allele-sharing model (Kong and Cox 1997). We note that the published Decode genetic map was originally constructed on the basis of the Haldane map function, or a no-interference model, but the distances were converted to Kosambi distances in the publication to make them directly comparable with the Marshfield map (Broman et al. 1998). However, Allegro, like many other multipoint linkage programs, can only process a no-interference model. Hence, our calculations here were based on the originally estimated Haldane map, but the results are presented with the locations converted to the published Kosambi map to ease referencing. Positions of markers not in the Decode map were set by interpolation on the basis of physical distances. Families were weighted halfway on the log scale between weighting families equally and weighting all pairs of affected relatives equally. This scheme gives weights similar to those proposed by Weeks and Lange (1988) as an extension of the scheme Hodge (1984) designed for sibships, and we have been using it as the default (see, e.g., Gretarsdottir et al. [2002]). Exact P values were calculated by comparing the observed LOD score with its complete data sampling distribution under the null hypothesis (Gudbjartsson et al. 2000), where a linkage result is considered significant if the single test P value is <2×10-5 (Lander and Kruglyak 1995). We have extended our linkage analysis program, Allegro, to include an imprinting-based scoring function. The extension allows us to assign weights to allele sharing specific to parental origins. For example, to investigate paternal imprinting, the scoring functions considers only the sharing of alleles transmitted to two affected relatives through their fathers. When these imprinting-based scoring functions were used, sex-specific genetic maps (Kong et al. 2002) were used in the calculations.


The prevalence of PsA was ∼20% in our study group (178 out of 906 patients). Using our genealogy database and patients related to up to and including seven meioses, we were able to connect 100 of these patients, 41 males (41%), and 59 females (59%), into 39 families for linkage analysis. Of these 100 patients, 45 and 50, respectively, were informative for linkage when pairs of affected individuals related only through their fathers and pairs related only through their mothers were used. After the addition of extra markers, the strongest evidence for linkage was observed on chromosome 16, with a LOD score of 2.17 at the marker D16S3038, which is located 75.62 cM from the p telomere of chromosome 16 (fig. 1). D16S3110, a marker we have mapped to within 1 Mb of D16S3038, has been reported elsewhere as marking a suggestive locus for psoriasis (Nair et al. 2000), and both of these markers are within 20 Mb of the NOD2 gene (MIM 605956), mapped to around 60.4 cM on the Decode map, thought to confer risk for inflammatory bowel disease (Hugot et al. 2001; Ogura et al. 2001). Linkage analysis using only paternal transmissions to affected individuals gave a maximum LOD score of 4.19 at marker D16S267; that is, at 81.25 cM from the p telomere of chromosome 16 or within 6 cM of our highest linkage marker for the entire cohort (fig. 2). The exact P value for this result was 5.31×10−6, which was still significant after adjustment for multiple testing because of the three linkage scans performed. The markers demarcating the 1-LOD drop are D16S3393 (82.7 cM from the p telomere) and D16S3089 (79.5 cM from the p telomere). All markers used in this analysis are available on request. When considering maternal transmissions only, the maximum LOD score was 1.03 at marker D16S3089 (fig. 2), which we genetically mapped to 4 cM telomeric of D16S3038, as mentioned above. We note in our ongoing study of psoriasis, as opposed to PsA, that there is currently no evidence for linkage to this location (data not shown).

Figure  1
Genome scan of 39 families with PsA with 1,000-microsatellite framework marker set, in addition to the fine mapping markers in all locations of interest. The multipoint LOD score is shown on the vertical axis; the distance from the p-terminal end of the ...
Figure  2
Linkage result of 39 families on chromosome 16 with additional markers and considering paternal transmissions only (black line) and maternal transmissions only (red line). The multipoint LOD score is shown on the vertical axis; the distance from the p-terminal ...


Genetic imprinting in human disease, a phenomenon involving a preferential paternal or maternal inheritance of a susceptibility allele to affected individuals, has been suggested in several complex genetic diseases (Lee et al. 2000; Cichon et al. 2001; Naumova et al. 2001; Strauch et al. 2001; Alcolado et al. 2002; DeLisi et al. 2002; Lindsay et al. 2002; Vandenbroeck et al. 2002) and is well established in some rarer diseases, such as the Prader-Willi and Angelman syndromes (Christian et al. 1998; Mann and Bartolomei 1999). Parental imprinting has also been suggested for several complex genetic diseases from an epidemiological standpoint (Lichter et al. 1995; Kato et al. 1996; Eapen et al. 1997; Haghighi et al. 1999; Rahman et al. 1999; Meigs et al. 2000). There is also suggestive evidence from linkage analysis, reported elsewhere, of common diseases and phenotypes where LOD scores increase or decrease when the analysis is conditioned on parental transmission. These include noninsulin-dependent diabetes mellitus, atopic dermatitis, bipolar disease, insulin-dependent diabetes mellitus (IDDM), schizophrenia, Crohn disease, and birth weight (Akolkar et al. 1997; Lee et al. 2000; Meigs et al. 2000; Cichon et al. 2001; Lindsay et al. 2001, 2002). However, in almost all of these and other linkage scans, conditioning on parental transmission, the interpretation of the existence of imprinted disease genes, must be tempered by the fact that almost none of the loci met the criteria for statistical significance, even without correction for the testing of multiple models. Of particular interest here is one linkage scan on psoriasis that showed an increased paternal transmission at the MHC susceptibility region (Burden et al. 1998), although we have not observed this phenomenon for any of the loci that we find contributing to the skin manifestations of psoriasis in Iceland.

Our findings support at the molecular genetic level the recent epidemiological observation that paternal imprinting might play a role in PsA (Rahman et al. 1999). Reanalysis of an IDDM genome scan performed in the United Kingdom (Mein et al. 1998) showed a paternal inheritance factor at D16S3098, which maps to within 20 Mb of our locus on 16q, with a LOD score of 1.81 for male meioses and a LOD score of 0.33 for female meioses at the same locus (Paterson et al. 1999). These results are interesting, although they are far from reaching statistical significance. The LOD score of 4.19 we observe at this location, however, exceeds the accepted criteria for genomewide significance and provides the first indication of a location for a non-MHC gene predisposing to PsA.

The position of the locus we report here is also interesting considering that a locus on chromosome 16q has been implicated in psoriasis elsewhere (Nair et al. 1997) and in Crohn disease. The Crohn disease susceptibility factor consists of an insertion mutation and several missense mutations in the NOD2 gene (which we map to 21 cM from our highest linkage marker) that have been identified in a subset of patients (Hugot et al. 2001; Ogura et al. 2001). This insertion causes a truncation of the NOD2 product that may lead to abnormal NF-κB responses to certain bacterial products (Lesage et al. 2002).

It has also been reported in an epidemiological study that the inheritance of Crohn disease may be influenced by parental imprinting (Akolkar et al. 1997). Patients with Crohn disease have approximately sevenfold increased risk of developing psoriasis, and they are at risk for a seronegative polyarthritis themselves (Lee et al. 1990; Nair et al. 1997), but the insertion mutation in the NOD2 gene observed in Crohn disease has not been found in psoriasis (Nair et al. 2001). It is possible that other variants of the NOD2 gene may be involved in psoriasis or a gene that is closely linked to NOD2. Our PsA cohort has not been screened for the known mutations in the NOD2 gene.

The peak we observe on chromosome 16 overlaps with a peak we have observed in families with osteoarthritis (OA) (data not shown). It is also, therefore, possible that what we are observing is a gene that causes susceptibility to joint afflictions. On the one hand, it may lead to OA when other susceptibility factors (trauma or other genetic factors) are present, and on the other hand, it may lead to PsA when factors predisposing to psoriasis are present. Our study shows the importance of the ability to link large numbers of patients together as we have done using our genealogy database. Additionally, looking at parental effects on the inheritance of phenotypes may add a new dimension to previous or future linkage scans, as we have found in this case.


We thank patients and their families for their participation, which made this study possible. We also thank the Association of Psoriasis and Eczema Patients in Iceland for their help in recruiting patients.

Electronic-Database Information

Accession numbers and URLs for data presented herein are as follows:

Online Mendelian Inheritance in Man (OMIM), http://www.ncbi.nlm.nih.gov/Omim/ (for psoriasis [MIM 177900] and NOD2 [MIM 605956])
Center for Medical Genetics, Marshfield Medical Research Foundation, http://research.marshfieldclinic.org/genetics/


Akolkar PN, Gulwani-Akolkar B, Heresbach D, Lin XY, Fisher S, Katz S, Silver J (1997) Differences in risk of Crohn's disease in offspring of mothers and fathers with inflammatory bowel disease. Am J Gastroenterol 92:2241–2244 [PubMed]
Alcolado JC, Laji K, Gill-Randall R (2002) Maternal transmission of diabetes. Diabet Med 19:89–98 [PubMed]
Al-Heresh AM, Proctor J, Jones SM, Dixey J, Cox B, Welsh K, McHugh N (2002) Tumour necrosis factor-alpha polymorphism and the HLA-Cw*0602 allele in psoriatic arthritis. Rheumatology 41:525–530 [PubMed]
Baker BS, Swain AF, Fry L, Valdimarsson H (1984) Epidermal T lymphocytes and HLA-DR expression in psoriasis. Br J Dermatol 110:555–564 [PubMed]
Balendran N, Clough RL, Arguello JR, Barber R, Veal C, Jones AB, Rosbotham JL, Little AM, Madrigal A, Barker JN, Powis SH, Trembath RC (1999) Characterization of the major susceptibility region for psoriasis at chromosome 6p21.3. J Invest Dermatol 113:322–328 [PubMed]
Broman KW, Murray JC, Sheffield VC, White RL, Weber JL (1998) Comprehensive human genetic maps: individual and sex-specific variation in recombination. Am J Hum Genet 63:861–869 [PMC free article] [PubMed]
Bruce IN, Silman AJ (2001) The aetiology of psoriatic arthritis. Rheumatology 40:363–366 [PubMed]
Burden AD, Javed S, Bailey M, Hodgins M, Connor M, Tillman D (1998) Genetics of psoriasis: paternal inheritance and a locus on chromosome 6p. J Invest Dermatol 110:958–960 [PubMed]
Christian SL, Bhatt NK, Martin SA, Sutcliffe JS, Kubota T, Huang B, Mutirangura A, Chinault AC, Beaudet AL, Ledbetter DH (1998) Integrated YAC contig map of the Prader-Willi/Angelman region on chromosome 15q11-q13 with average STS spacing of 35 kb. Genome Res 8:146–157 [PMC free article] [PubMed]
Cichon S, Schumacher J, Muller DJ, Hurter M, Windemuth C, Strauch K, Hemmer S, et al (2001) A genome screen for genes predisposing to bipolar affective disorder detects a new susceptibility locus on 8q. Hum Mol Genet 10:2933–2944 [PubMed]
Costello P, FitzGerald O (2001) Disease mechanisms in psoriasis and psoriatic arthritis. Curr Rheumatol Rep 3:419–427 [PubMed]
DeLisi LE, Shaw SH, Crow TJ, Shields G, Smith AB, Larach VW, Wellman N, Loftus J, Nanthakumar B, Razi K, Stewart J, Comazzi M, Vita A, Heffner T, Sherrington R (2002) A genome-wide scan for linkage to chromosomal regions in 382 sibling pairs with schizophrenia or schizoaffective disorder. Am J Psychiatry 159:803–812 [PubMed]
Eapen V, O'Neill J, Gurling HM, Robertson MM (1997) Sex of parent transmission effect in Tourette's syndrome: evidence for earlier age at onset in maternally transmitted cases suggests a genomic imprinting effect. Neurology 48:934–937 [PubMed]
Eastmond CJ (1994) Psoriatic arthritis: genetics and HLA antigens. Baillieres Clin Rheumatol 8:263–276 [PubMed]
Elder JT, Nair RP, Henseler T, Jenisch S, Stuart P, Chia N, Christophers E, Voorhees JJ (2001) The genetics of psoriasis 2001: the odyssey continues. Arch Dermatol 137:1447–1454 [PubMed]
Farber EM, Nall L, Watson W (1974) Natural history of psoriasis in 61 twin pairs. Arch Dermatol 109:207–211 [PubMed]
Fearon U, Veale DJ (2001) Pathogenesis of psoriatic arthritis. Clin Exp Dermatol 26:333–337 [PubMed]
Gladman DD, Farewell VT, Rahman P, Schentag CT, Pellett F, Ng CM, Wade JA (2001) HLA-DRB1*04 alleles in psoriatic arthritis: comparison with rheumatoid arthritis and healthy controls. Hum Immunol 62:1239–1244 [PubMed]
Gonzalez S, Brautbar C, Martinez-Borra J, Lopez-Vazquez A, Segal R, Blanco-Gelaz MA, Enk CD, Safriman C, Lopez-Larrea C (2001) Polymorphism in MICA rather than HLA-B/C genes is associated with psoriatic arthritis in the Jewish population. Hum Immunol 62:632–638 [PubMed]
Gonzalez S, Martinez-Borra J, Lopez-Vazquez A, Garcia-Fernandez S, Torre-Alonso JC, Lopez-Larrea C (2002) MICA rather than MICB, TNFA, or HLA-DRB1 is associated with susceptibility to psoriatic arthritis. J Rheumatol 29:973–978 [PubMed]
Gretarsdottir S, Sveinbjornsdottir S, Jonsson HH, Jakobsson F, Einarsdottir E, Agnarsson U, Shkolny D, et al (2002) Localization of a susceptibility gene for common forms of stroke to 5q12. Am J Hum Genet 70:593–603 [PMC free article] [PubMed]
Gudbjartsson DF, Jonasson K, Frigge ML, Kong A (2000) Allegro, a new computer program for multipoint linkage analysis. Nat Genet 25:12–13 [PubMed]
Gudjonsson JE, Karason A, Antonsdottir A, Runarsdottir H, Gulcher JR, Stefansson K, Valdimarsson H (2002) HLA-Cw6 positive and HLA-Cw6 negative patients with psoriasis vulgaris have distinct clinical features. J Invest Dermatol 118:362–365 [PubMed]
Gulcher J, Stefansson K (1998) Population genomics: laying the groundwork for genetic disease modeling and targeting. Clin Chem Lab Med 36:523–527 [PubMed]
Gulcher JR, Kristjansson K, Gudbjartsson H, Stefansson K (2000) Protection of privacy by third-party encryption in genetic research in Iceland. Eur J Hum Genet 8:739–742 [PubMed]
Haghighi F, Fyer AJ, Weissman MM, Knowles JA, Hodge SE (1999) Parent-of-origin effect in panic disorder. Am J Med Genet 88:131–135 [PubMed]
Hodge SE (1984) The information contained in multiple sibling pairs. Genet Epidemiol 1:109–122 [PubMed]
Hugot J-P, Chamaillard M, Zouali H, Lesage S, Cézard J-P, Belaiche J, Almer S, Tysk C, O'Morain CA, Gassull M, Binder V, Finkel Y, Cortot A, Modigliani R, Laurent-Puig P, Gower-Rousseau C, Macry J, Colombel JF, Sahbatou M, Thomas G (2001) Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease. Nature 411:599–603 [PubMed]
Jenisch S, Henseler T, Nair RP, Guo SW, Westphal E, Stuart P, Kronke M, Voorhees JJ, Christophers E, Elder JT (1998) Linkage analysis of human leukocyte antigen (HLA) markers in familial psoriasis: strong disequilibrium effects provide evidence for a major determinant in the HLA-B/-C region. Am J Hum Genet 63:191–199 [PMC free article] [PubMed]
Kato T, Winokur G, Coryell W, Keller MB, Endicott J, Rice J (1996) Parent-of-origin effect in transmission of bipolar disorder. Am J Med Genet 67:546–550 [PubMed]
Kong A, Cox NJ (1997) Allele-sharing models: LOD scores and accurate linkage tests. Am J Hum Genet 61:1179–1188 [PMC free article] [PubMed]
Kong A, Gudbjartsson DF, Sainz J, Jonsdottir GM, Gudjonsson SA, Richardsson B, Sigurdardottir S, Barnard J, Hallbeck B, Masson G, Shlien A, Palsson ST, Frigge ML, Thorgeirsson TE, Gulcher JR, Stefansson K (2002) A high-resolution recombination map of the human genome. Nat Genet 31:241–247 [PubMed]
Kruglyak L, Daly MJ, Reeve-Daly MP, Lander ES (1996) Parametric and nonparametric linkage analysis: a unified multipoint approach. Am J Hum Genet 58:1347–1363 [PMC free article] [PubMed]
Lander E, Kruglyak L (1995) Genetic dissection of complex traits: guidelines for interpreting and reporting linkage results. Nat Genet 11:241–247 [PubMed]
Lee FI, Bellary SV, Francis C (1990) Increased occurrence of psoriasis in patients with Crohn's disease and their relatives. Am J Gastroenterol 85:962–963 [PubMed]
Lee YA, Wahn U, Kehrt R, Tarani L, Businco L, Gustafsson D, Andersson F, Oranje AP, Wolkertstorfer A, Berg AV, Hoffmann U, Kuster W, Wienker T, Ruschendorf F, Reis A (2000) A major susceptibility locus for atopic dermatitis maps to chromosome 3q21. Nat Genet 26:470–473 [PubMed]
Lesage S, Zouali H, Cezard J-P and the EPWG-IBD Group, Colombel JF and the EPIMAD Group, Belaiche J and the GETAID Group, Almer S, Tysk C, O'Morain C, Gassull M, Binder V, Finkel Y, Modigliani R, Gower-Rousseau C, Macry J, Merlin F, Chamaillard M, Jannot AS, Thomas G, Hugot J-P (2002) CARD15/NOD2 mutational analysis and genotype-phenotype correlation in 612 patients with inflammatory bowel disease. Am J Hum Genet 70:845–857 [PMC free article] [PubMed]
Lichter DG, Jackson LA, Schachter M (1995) Clinical evidence of genomic imprinting in Tourette's syndrome. Neurology 45:924–928 [PubMed]
Lindsay RS, Kobes S, Knowler WC, Bennett PH, Hanson RL (2001) Genome-wide linkage analysis assessing parent-of-origin effects in the inheritance of type 2 diabetes and BMI in Pima Indians. Diabetes 50:2850–2857 [PubMed]
Lindsay RS, Kobes S, Knowler WC, Hanson RL (2002) Genome-wide linkage analysis assessing parent-of-origin effects in the inheritance of birth weight. Hum Genet 110:503–509 [PubMed]
Mann MR, Bartolomei MS (1999) Towards a molecular understanding of Prader-Willi and Angelman syndromes. Hum Mol Genet 8:1867–1873 [PubMed]
Meigs JB, Cupples LA, Wilson PW (2000) Parental transmission of type 2 diabetes: the Framingham Offspring Study. Diabetes 49:2201–2207 [PubMed]
Mein CA, Esposito L, Dunn MG, Johnson GC, Timms AE, Goy JV, Smith AN, Sebag-Montefiore L, Merriman ME, Wilson AJ, Pritchard LE, Cucca F, Barnett AH, Bain SC, Todd JA (1998) A search for type 1 diabetes susceptibility genes in families from the United Kingdom. Nat Genet 19:297–300 [PubMed]
Moll JM, Wright V (1973a) Psoriatic arthritis. Semin Arthritis Rheum 3:55–78 [PubMed]
——— (1973b) Familial occurrence of psoriatic arthritis. Ann Rheum Dis 32:181–201 [PMC free article] [PubMed]
Nair RP, Henseler T, Jenisch S, Stuart P, Bichakjian CK, Lenk W, Westphal E, Guo SW, Christophers E, Voorhees JJ, Elder JT (1997) Evidence for two psoriasis susceptibility loci (HLA and 17q) and two novel candidate regions (16q and 20p) by genome-wide scan. Hum Mol Genet 6:1349–1356 [PubMed]
Nair RP, Stuart P, Henseler T, Jenisch S, Chia NV, Westphal E, Schork NJ, Kim J, Lim HW, Christophers E, Voorhees JJ, Elder JT (2000) Localization of psoriasis-susceptibility locus PSORS1 to a 60-kb interval telomeric to HLA-C. Am J Hum Genet 66:1833–1844 [PMC free article] [PubMed]
Nair RP, Stuart P, Ogura Y, Inohara N, Chia NVC, Young L, Henseler T, Jenisch S, Christophers E, Voorhees JJ, Nunez G, Elder JT (2001) Lack of association between NOD2 3020 InsC frameshift mutation and psoriasis. J Invest Dermatol 117:1671–1672 [PubMed]
Naumova AK, Greenwood CM, Morgan K (2001) Imprinting and deviation from Mendelian transmission ratios. Genome 44:311–320 [PubMed]
Ogura Y, Bonen DK, Inohara N, Nicolae DL, Chen FF, Ramos R, Britton H, Moran T, Karaliuskas R, Duerr RH, Achkar JP, Brant SR, Bayless TM, Kirschner BS, Hanauer SB, Nunez G, Cho JH (2001) A frameshift mutation in NOD2 associated with susceptibility to Crohn's disease. Nature 411:603–606 [PubMed]
Oka A, Tamiya G, Tomizawa M, Ota M, Katsuyama Y, Makino S, Shiina T, Yoshitome M, Iizuka M, Sasao Y, Iwashita K, Kawakubo Y, Sugai J, Ozawa A, Ohkido M, Kimura M, Bahram S, Inoko H (1999) Association analysis using refined microsatellite markers localizes a susceptibility locus for psoriasis vulgaris within a 111 kb segment telomeric to the HLA-C gene. Hum Mol Genet 8:2165–2170 [PubMed]
Patel S, Veale D, FitzGerald O, McHugh NJ (2001) Psoriatic arthritis—emerging concepts. Rheumatology 40:243–246 [PubMed]
Paterson AD, Naimark DM, Petronis A (1999) The analysis of parental origin of alleles may detect susceptibility loci for complex disorders. Hum Hered 49:197–204 [PubMed]
Prinz JC (1999) Which T cells cause psoriasis? Clin Exp Dermatol 24:291–295 [PubMed]
Rahman P, Gladman DD, Schentag CT, Petronis A (1999) Excessive paternal transmission in psoriatic arthritis. Arthritis Rheum 42:1228–1231 [PubMed]
Rahman P, Schentag CT, Beaton M, Gladman DD (2000) Comparison of clinical and immunogenetic features in familial versus sporadic psoriatic arthritis. Clin Exp Rheumatol 18:7–12 [PubMed]
Samuelsson L, Enlund F, Torinsson A, Yhr M, Inerot A, Enerback C, Wahlstrom J, Swanbeck G, Martinsson T (1999) A genome-wide search for genes predisposing to familial psoriasis by using a stratification approach. Hum Genet 105:523–529 [PubMed]
Strauch K, Bogdanow M, Fimmers R, Baur MP, Wienker TF (2001) Linkage analysis of asthma and atopy including models with genomic imprinting. Genet Epidemiol Suppl 1:S204–S209 [PubMed]
Tiilikainen A, Lassas A, Karvonen J, Vartianen P, Julin M (1980) Psoriasis and HLA-Cw6. Br J Dermatol 102:179–184 [PubMed]
Trembath RC, Clough RL, Rosbotham JL, Jones AB, Camp RD, Frodsham A, Browne J, Barber R, Terwilliger J, Lathrop GM, Barker JN (1997) Identification of a major susceptibility locus on chromosome 6p and evidence for further disease loci revealed by two stage genome wide search in psoriasis. Hum Mol Genet 6:813–820 [PubMed]
Valdimarsson H, Baker BS, Jonsdottir I, Powles A, Fry L (1995) Psoriasis: a T-cell-mediated autoimmune disease induced by streptococcal superantigens? Immunol Today 16:145–149 [PubMed]
Vandenbroeck K, Fiten P, Heggarty S, Goris A, Cocco E, Hawkins SA, Graham CA, Marrosu MG, Opdenakker G (2002) Chromosome 7q21-22 and multiple sclerosis: evidence for a genetic susceptibility effect in vicinity to the protachykinin-1 gene. J Neuroimmunol 125:141–148 [PubMed]
Weeks DE, Lange K (1988) The affected-pedigree-member method of linkage analysis. Am J Hum Genet 42:315–326 [PMC free article] [PubMed]
Winchester R (1995) Psoriatic arthritis. Dermatol Clin 13:779–792 [PubMed]

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    Genome Survey Sequence (GSS) nucleotide records reported in the current articles.
  • PubMed
    PubMed citations for these articles

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