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Effect of CBA/N xid on Spontaneous Production of Antibodies to DNA in MRL/1 and NZB Backcross Mice (1980)

COWDERY, J. S. ; TAUROG, J. D. ; STEINBERG, A. D.

Oxford, UK : Blackwell Publishing Ltd

Scandinavian journal of immunology 12 (1980), S. 0

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ISSN: 1365-3083

Source: Blackwell Publishing Journal Backfiles 1879-2005

Topics: Medicine

Notes: We have used the CBA/N X-linked B-cell maturation defect (xid) as a probe to analyse the B-cell subset involved in spontaneous anti-DNA production in MRL/1 and NZB mice. The presence of xid in NZB offspring significantly suppressed anti-DNA production, whereas it did not suppress spontaneously produced antibody to DNA in MRL/1 offspring. These studies suggest that largely non-overlapping B-cell subsets are responsible for the spontaneous production of anti-DNA in MRL/1 and NZB mice.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1111/j.1365-3083.1980.tb00097.x

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A high incidence of Shigella-induced arthritis in a primate species: major histocompatibility complex class I molecules associated with resistance and susceptiblity, and their relationship to HLA-B27 (2000)

Urvater, J. A. ; McAdam, S. N. ; Loehrke, J. H. ; [et al.]

Springer

Immunogenetics 51 (2000), S. 314-325

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ISSN: 1432-1211

Keywords: Key words Nonhuman primate ; Spondyloarthropathy ; Reactive arthritis ; Autoimmunity ; Major histocompatibility locus

Source: Springer Online Journal Archives 1860-2000

Topics: Biology , Medicine

Notes: Abstract The human major histocompatibility complex (MHC) class I gene, HLA-B27, is a strong risk factor for susceptibility to a group of disorders termed spondyloarthropathies. Rodents that express HLA-B27 develop spondyloarthropathies, implicating HLA-B27 in the etiology of these disorders. To determine whether an HLA-B27-like molecule was associated with spondyloarthropathies in nonhuman primates, we analyzed the MHC class I cDNAs expressed in a cohort of rhesus macaques that developed reactive arthritis after an outbreak of shigellosis. We identified several cDNAs with only limited sequence similarity to HLA-B27. Interestingly, one of these MHC molecules had a B pocket identical to that of HLA-B39. Pool sequencing of radiolabeled peptides bound by this molecule demonstrated that, like HLA-B27 and HLA-B39, it could bind peptides with arginine at the second position. However, extensive analysis of the MHC class I molecules in this cohort revealed no statistically significant association between any particular MHC class I allele and susceptibility to reactive arthritis. Furthermore, none of the rhesus MHC class I molecules bore a strong resemblance to HLA-B27, indicating that reactive arthritis can develop in this animal model in the absence of an HLA-B27-like molecule. Surprisingly, there was a statistically significant association between the rhesus macaque MHC A locus allele, Mamu-A*12, and the absence of reactive arthritis following Shigella infection.