Basic information of RT1-A3 :
| Official Symbol of Gene | RT1-A3 |
| Species | Rattus norvegicus (Norway rat) |
| Entrez Gene ID | 309627 |
| Official Full Name | RT1 class I, locus A3 |
| Also known as | RT1; RT1-A; RT1.A3; RT1-A3n |
| Gene Type | protein coding |
| dbXrefs | RGD:1359610 |
| Map Location | 20p12 |
| Variation Type | haplotype |
| refSNP ID | N/A |
Sample information of multiple sclerosis:
| Detected Sample | brain and spinal cord sections |
| Sample Detail | N/A |
| Detected Method | a microsatellite marker located within the RT1 region |
| Disease | EAE |
| Disease subtype | N/A |
| Population | female rats ACI rats，PVG-RT1，BN rats，DA, DA.1H, LEW, LEW.1A, LEW.1AV1,and LEW.1W，LEW.1N, LEW.1AR1, LEW.1AR2, LEW.1WR1,LEW.1WR2 rat |
| Sample Size | N/A |
Literature information of multiple sclerosis :
| Pubmed ID | 9739061 |
| Year | 1998 |
| Title | MHC haplotype-dependent regulation of MOG-induced EAE in rats. |
Results of multiple sclerosis :
| Risk Type | Phenotypic risk |
| Main Result | Positive |
| Result | MHC haplotypes differ in the severity of the ensuing disease they permit in response to a constant autoantigenic MOG challenge. Furthermore, the MHC haplotype determines the amount of autoantigen needed to induce disease. Thus, MHC haplotypes are not strictly disease permissive or resistant.Instead, there is a hierarchy in MHC haplotype regulation of disease, with high responder haplotypes such as RT1n and RT1h, intermediate ones such as RT1a ,RT1av1, RT1r3, and RT1r6, and low responders such as RT1u,RT1r2, RT1r4, and RT1l. Notably, no single haplotype is completely protected.An increase in numbers of IFN-g mRNA-expressing cells was recorded only in the disease-susceptible LEW.1AV1 and DA rat strains, although all four strains displayed similar increases after mitogenic stimulation with Con A. The numbers of anti-MOG Ab-secreting cells were also higher in DA rats and LEW.1AV1 rats than in PVGRT1a rats and ACI rats. The RT1av1 haplotype is permissive for induction of a MOG-specific autoimmune response in all strains, but the functional maturation of this response is strongly influenced by non-MHC genes. |
| Mechanism/Pathway | This study strongly suggests that the mechanism for MHC haplotype regulation of the degree of ensuing disease is by regulation of the quantity and quality of the autoimmune response after autoantigenic challenge, since these factors directly correlated to each other. |
