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Results: 4

1.
Fig. 1

Fig. 1. From: Unravelling the genetic complexity of autoimmune thyroid disease: HLA, CTLA-4 and beyond.

Simplified version of how Th1 and Th2 responses lead to the different clinical presentations of AITD.

M J SIMMONDS, et al. Clin Exp Immunol. 2004 April;136(1):1-10.
2.
Fig. 4

Fig. 4. From: Unravelling the genetic complexity of autoimmune thyroid disease: HLA, CTLA-4 and beyond.

Association of SNPs within the CD28-CTLA4-ICOS gene region with GD. When association with GD was plotted for all the SNPs, a region consisting of CTLA-4 and 5′ ICOS gene (CTLA4 LD BLOCK) was believed to contain the aetiological variant. This diagram highlights the CT60—JO30-JO31-J027–1 peak of linkage that is believed to contain the aetiological variant associated with GD and HT (reprinted by permission from Nature 2003; 423:506–511. Copyright 2003, Macmillan Publishers Ltd.)

M J SIMMONDS, et al. Clin Exp Immunol. 2004 April;136(1):1-10.
3.
Fig. 2

Fig. 2. From: Unravelling the genetic complexity of autoimmune thyroid disease: HLA, CTLA-4 and beyond.

(a) HLA class I gene region. (b) HLA class II gene region with known haplotypes associated with GD and HT (transport associated with antigen processing genes (TAP1 and TAP2) and large multifunctional protein (LMP)). (c) HLA class II gene regions (Heat shock protein (HSP), tumour necrosis factor (TNF))

M J SIMMONDS, et al. Clin Exp Immunol. 2004 April;136(1):1-10.
4.
Fig. 3

Fig. 3. From: Unravelling the genetic complexity of autoimmune thyroid disease: HLA, CTLA-4 and beyond.

The stimulatory pathway of CD28 and the antagonist effect of CTLA-4 on Th cell activation. T cell activation occurs via a two stage process. Stage 1 involves generation of a signal via the interaction of a presented antigen with the TCR-CD3 complex. Stage 2 of T cell activation involves a costimulatory signal from CD28 interaction with B7. Regulation of this second stage of T cell activation is provided by a down regulation of T cell activation by CTLA-4. Due to the negative control function of CTLA-4, functional mutations in this gene could increase susceptibility to autoimmune thyroid disease.

M J SIMMONDS, et al. Clin Exp Immunol. 2004 April;136(1):1-10.

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