Results: 5

1.
Figure 2

Figure 2. From: Experimental Autoimmune Breast Failure.

α-Lactalbumin immunization causes infiltration of CD3+ T cells in lactating breast tissue only. Immunohistochemical analysis shows numerous CD3+ T cells clustered in periductal areas (arrows) of breast tissues from lactating mice immunized with α-lactalbumin 6 to 7 weeks before initiation of lactation (top left panel). Clusters of CD3+ T cells were not observed in breast tissues from lactating mice immunized with CFA (top right panel) or in nonlactating mice immunized with either α-lactalbumin (bottom left panel) or CFA (bottom right panel). Scale bars: 50 μm.

Pavani Kesaraju, et al. Am J Pathol. 2012 September;181(3):775-784.
2.
Figure 3

Figure 3. From: Experimental Autoimmune Breast Failure.

Altered gene expression in lactating breast tissues from α-lactalbumin–immunized mice. Six weeks after immunization with either α-lactalbumin or CFA alone, total RNA from lactating mammary tissue was analyzed for gene expression by real-time qRT-PCR. A: Lactating breast tissue from α-lactalbumin–immunized mice showed significantly elevated gene expression levels of IFN-γ (P = 0.001) but not IL-10 (P > 0.10) and significantly increased gene expression of α-lactalbumin (P < 0.002) and α-casein (P = 0.0008). Asterisks indicate significance. B: α-Lactalbumin and α-casein gene expression levels were not elevated in nonlactating breast tissue from α-lactalbumin–immunized mice. C: Except for the spleen, IFN-γ gene expression levels were not elevated in any tissues examined from normal nonlactating α-lactalbumin–immunized mice. Data are given as mean ± SE.

Pavani Kesaraju, et al. Am J Pathol. 2012 September;181(3):775-784.
3.
Figure 5

Figure 5. From: Experimental Autoimmune Breast Failure.

Passive transfer of autoimmune breast failure with primed T cells. Lactating female SWXJ mice were injected i.p. with LNCs, CD4+ T cells, CD8+ T cells, B cells, or sera from mice immunized previously with either recombinant α-lactalbumin or recombinant cochlin in CFA. After weaning (approximately 3 to 4 weeks after transfer), mice were euthanized for molecular analysis of tissues. A: Inhibition of growth did not occur in pups from mothers that received B cells (P > 0.50; left panel) or sera (P > 0.60; middle panel) from α-lactalbumin–immunized mice but did occur in pups from mothers that received α-lactalbumin–activated LNCs (P < 0.04; right panel). B: Significantly elevated α-casein gene expression, a surrogate marker for breast failure, did not occur in lactating breast tissues from control females receiving cochlin-activated LNCs (P > 0.10) but did occur in lactating breast tissues from females receiving α-lactalbumin–activated LNCs (P = 0.02), CD4+ T cells (P = 0.03), or CD8+ T cells (P = 0.02). Data are given as mean ± SE. Asterisks indicate significance. In all experiments, n = 6.

Pavani Kesaraju, et al. Am J Pathol. 2012 September;181(3):775-784.
4.
Figure 4

Figure 4. From: Experimental Autoimmune Breast Failure.

Functional phenotype of autoimmune breast failure. Four weeks after immunization with either α-lactalbumin or CFA alone, females were mated with identical males, and the resultant litters were examined daily for differences in mean pup weight. A: Pups from α-lactalbumin–immunized mothers consistently showed a failure to thrive as measured by significantly decreased mean pup weights over several mating cycles (P < 0.04 for every individual mating). Asterisks indicate significance. B: There were no significant differences (P > 0.60) in mean number of mice per litter between females immunized with α-lactalbumin or CFA alone. Nourishment failure often presented with kwashiorkor-like signs, including alopecia (three pups on the left) (C) and liver toxicity as indicated by increased serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT) levels (D). Data are given as mean ± SE.

Pavani Kesaraju, et al. Am J Pathol. 2012 September;181(3):775-784.
5.
Figure 1

Figure 1. From: Experimental Autoimmune Breast Failure.

α-Lactalbumin immunization induces a proinflammatory type-1 immune response. A: Western blot analysis to detect His-tagged mouse α-lactalbumin. Arrows show the positions of the α-lactalbumin monomer and dimer. Positions of molecular weight markers are indicated on the left side of the gel. B: SWXJ female mice were immunized with 150 μg of recombinant mouse α-lactalbumin in CFA. Ten days later, LNCs showed antigen-specific proliferation in recall responses over a broad dose range to α-lactalbumin but not to recombinant human cochlin, an irrelevant control antigen cloned and purified in an identical manner. C: ELISA of culture supernatants from 10-day LNCs stimulated with 20 μg/mL of α-lactalbumin showed production of the type 1 proinflammatory cytokines IFN-γ and IL-2 with minimal production of the type 2 regulatory cytokines IL-5 and IL-10. D: Recall responses to 20 μg/mL of α-lactalbumin were elicited from CD4+ and CD8+ T cells purified by magnetic bead separation from LNCs 10 days after immunization with α-lactalbumin. Data are given as mean ± SE.

Pavani Kesaraju, et al. Am J Pathol. 2012 September;181(3):775-784.

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