Disease relevance of RT1-B

• To investigate the role of MHC in the development of rat Heymann nephritis (HN), an animal model of membranous nephropathy, a monoclonal antibody (mAb) specific to rat MHC class II antigen (RT1B) was administered, and its effectiveness in inhibiting HN was assessed [1].
• In comparison with experimental contact hypersensitivity to 2,4-dinitrofluorobenzene, we found a low expression of RT1B and RT1D [2].

High impact information on RT1-B

• Immunological properties of subcellular rat lymphocyte preparations. Primary allogeneic stimulation in vitro by fractions containing Ia (RT1-B), but not RT1-A antigens [3].
• Inhibition of lesion development was accompanied by expression of the class II histocompatibility (Ia) gene, RT1B, suggesting that both were directly related to the administration of gIFN [4].
• The encephalitogenic rat T cell clone C14 recognizes the myelin basic protein 69-89 peptide in the context of the RT1B major histocompatibility complex (MHC) class II molecule [5].
• Following DA skin grafting, there was an accelerated production of antibodies to whole, undenatured class I MHC molecules, even in the LEW rats preimmunized with RT1-B alpha and RT1-B beta chains [6].
• The uveitogenic lymphocyte line (ThS) stains positively for the ART 18 (IL-2 receptor) and W3/25 (T helper/inducer); negatively for OX6 (RT1B) and OX8 (T suppressor/cytotoxic cells) [7].

Biological context of RT1-B

• Classical RT1-A class I and RT1-B class II major histocompatibility complex (MHC) molecules were purified from DA (RT1avl) spleens, and the individual chains separated and purified by preparative polyacrylamide gel electrophoresis in sodium dodecyl sulfate [6].
• Each serological haplotype was unique at the nucleotide level of the sequenced RT1-B/D region [8].
• After DNA preparation from the lymphoid organs, RT1B beta domain 1 region was amplified by PCR, and RFLP analysis was performed with PvuII restriction enzyme [9].
• RT1B/D+ non-lymphoid DC in early GVHD and Hg-induced autoimmunity of rat salivary and lacrimal glands [10].

Anatomical context of RT1-B

• Finally, expression of RT1-B (Ia) but not ED-2 is reported to be typical of interstitial dendritic cells rather than tissue macrophages, suggesting a unique function for the glomerular and periglomerular macrophage infiltrate in this model [11].
• The RT1-B/D region-associated antigens which were serologically defined in the previous study (Ohhashi et al., 1981), were partially purified from membranes of a rat B cell leukaemia, KNL-14 [12].
• An immunohistochemical procedure was carried out on alternate, serial, cryostat sections with antibodies against CDllb (macrophages, dendritic cells) and class II major histocompatibility complex (MHC) molecules (RT1B) [13].
• RESULTS: Before the induction of EC, cells stained with OX6 (rat MHC class 2, RT1B), ED1 (tissue macrophages), ED2 (resident macrophages), CD4, or major basic protein were present in the peripheral corneal stroma [14].

Associations of RT1-B with chemical compounds

• The effect of cyclosporine on the alloantibody response to blood transfusion was investigated in inbred strains of rats by IHA and CELISA; recipient animals differed from the donors at the class I (RT1A) or both class I and class II (RT1B) antigens of the major histocompatibility complex [15].

Other interactions of RT1-B

• Here we describe the complementary DNA (cDNA) sequence encoding the alpha and beta chains of both the RT1-B and RT1-D locus genes of the rat RT1u haplotype [16].
• Hence, it is possible to generate Ia-related allogeneic helper signals in primary, as well as secondary, in vitro responses, using subcellular membrane fragments that have restricted expression of RT1-B-, but not RT1-A-, encoded antigens [3].
• The rat major histocompatibility complex loci RT1-B and RT1-D are equivalent to the human leucocyte antigens HLA-DQ and HLA-DR respectively [16].
• The LEJ(RT1-AuBb) inbred rat strain showed a low response to BI, indicating that Ir-BI is closer to RT1-B/RT1-D region than to RT1-A [17].

Analytical, diagnostic and therapeutic context of RT1-B

• Rat thymocyte membrane fractions have been prepared which exhibit strain-specific primary mixed-lymphocyte reaction (MLR)-stimulating and Ia (RT1-B) antigenic properties [3].
• In intra-MHC recombinant rat strains the element determining rejection or acceptance of the allograft mapped to the RT1-B/D-C/E/M region in PVG.R8 and PVG.R23 rats, in accordance with the patterns of NK alloreactivity in these strain combinations [18].
• Renal transplantation of RT1-B-matched, RT1-A-mismatched rats [19].
• Ultrastructural analysis, along with immunocytochemistry for RT1B (indicating the presence of MHCII) and using antibody against mononuclear phagocytes, showed the cells to be macrophages [20].
• METHODS: Age-matched Buffalo (RT1B) rats randomly assigned to 7 experimental groups received either a Lewis (RT1L) rat posterior tibial-sciatic nerve allograft or a Buffalo (RT1B) syngeneic isograft [21].

References