anti-rat CD8 (Clone: OX-8)
Haag, S., et al. (2015). "Positional identification of RT1-B (HLA-DQ) as susceptibility locus for autoimmune arthritis." J Immunol 194(6): 2539-2550. PubMed
Rheumatoid arthritis (RA) is associated with amino acid variants in multiple MHC molecules. The association to MHC class II (MHC-II) has been studied in several animal models of RA. In most cases these models depend on T cells restricted to a single immunodominant peptide of the immunizing Ag, which does not resemble the autoreactive T cells in RA. An exception is pristane-induced arthritis (PIA) in the rat where polyclonal T cells induce chronic arthritis after being primed against endogenous Ags. In this study, we used a mixed genetic and functional approach to show that RT1-Ba and RT1-Bb (RT1-B locus), the rat orthologs of HLA-DQA and HLA-DQB, determine the onset and severity of PIA. We isolated a 0.2-Mb interval within the MHC-II locus of three MHC-congenic strains, of which two were protected from severe PIA. Comparison of sequence and expression variation, as well as in vivo blocking of RT1-B and RT1-D (HLA-DR), showed that arthritis in these strains is regulated by coding polymorphisms in the RT1-B genes. Motif prediction based on MHC-II eluted peptides and structural homology modeling suggested that variants in the RT1-B P1 pocket, which likely affect the editing capacity by RT1-DM, are important for the development of PIA.
Camara, M., et al. (2013). "CD8(+) T cell help is required for efficient induction of EAE in Lewis rats." J Neuroimmunol 260(1-2): 17-27. PubMed
The role of CD8(+) T cells in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) is still unclear. We describe here significantly reduced disease activity of EAE both in Lewis rats depleted of CD8(+) T cells by monoclonal antibodies and CD8 knockout rats, which was accompanied by reduced leukocyte infiltration into the spinal cord. We detected myelin basic protein (MBP)-specific CD8(+) T cells in peripheral lymphoid organs of CD8-depleted animals which, however, failed to differentiate into interferon-gamma-producing effector cells. Our results indicate that CD8(+) T cells interact with myelin-specific CD8(+) T cells early in EAE enabling them to differentiate into pathogenic effector cells.