Polymorphisms of the tumor necrosis factor receptor type 1 locus among autoimmune susceptible and resistant inbred rat strains

• Published in: Immunogenetics (New York) Vol. 53; no. 5; pp. 427 - 429
• Main Authors: Furuya, T, Salstrom, J L, Joe, B, Hashiramoto, A, Dobbins, D E, Wilder, R L, Remmers, E F
• Format: Journal Article
• Language: English
• Published: United States 01-07-2001
• Subjects: Amino Acid Sequence; Animals; Antigens, CD - genetics; Arthritis - genetics; Arthritis - immunology; Autoimmune Diseases - genetics; chromosome 4; Chromosome Mapping; Molecular Sequence Data; Polymorphism, Genetic; Quantitative Trait, Heritable; Rats; Rats, Inbred Strains - genetics; Receptors, Tumor Necrosis Factor - genetics; Receptors, Tumor Necrosis Factor, Type I; Sequence Homology, Amino Acid; Tnfr1 protein; Tnfrsf1a gene; tumor necrosis factor receptors
• ISSN: 0093-7711; 1432-1211
• DOI: 10.1007/s002510100338

Among inbred rat strains, susceptibility to and severity of autoimmune diseases varies dramatically. For example, DA/Bkl (DA), LEW/NHsd (LEW), and BB/(DR)/Wor [BB(DR)] rats are susceptible to collagen-induced arthritis (CIA), and experimental arthritis model with many features that resemble rheumatoid arthritis (RA). By contrast, ACI/SegHsd (ACI), BN/SsNHsd (BN), and F344/NHsd (F344) rats are resistant to or develop only mild CIA. Such strain susceptibility patterns extend to other rodent autoimmune disease models in a similar fashion. DA and LEW rats are highly susceptible to experimental allergic encephalomyelitis and experimental autoimmune uveitis, whereas F344 and BN rats are relatively resistant to both diseases. We recently reported a significant quantitative trait locus (QTL) on rat chromosome (Chr) 4, Cia13, which regulated CIA severity in both F2(DAXBN) and F2[BB(DR)XBN] populations. The rat CIA13 region shows syntenic conservation with the 12p13.2 region of human Chr 12. This region contains a suggestive locus for RA and contains tumor necrosis factor (TNF) receptor superfamily member 1A (TNFRSF1A), which is associated with periodic-fever syndomes. These observations suggest that the TNFRSF1A locus may influence susceptibility to several inflammatory diseases, and raise the possibility that this locus might account for differences in CIA susceptibility and/or severity among rat strains.