Literature DB >> 6271873

Ir gene control of the cytotoxic T lymphocyte response to Sendai virus: H-2k mice are low responders to Sendai.

M E Shapiro, S J Burakoff, B Benacerraf, R W Finberg.   

Abstract

H-2k mice generate a secondary in vitro cytotoxic T lymphocyte response to Sendai virus 20- to 100-fold weaker than those of other haplotypes tested (H-2b,d,q,s). This immune response defect maps to both H-2K and H-2D. H-2k x H-2d F1 mice (responder x nonresponder) only lyse targets that have the d allele at H-2K and/or H-2D. H-2k targets are equally lysable with anti-Sendai antibody. Furthermore, H-2k mice demonstrate normal antibody and T cell proliferation responses to Sendai virus. The Ir gene defect therefore appears to be limited to the generation of the cytotoxic T lymphocytes.

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Year:  1981        PMID: 6271873

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  3 in total

1.  Alternative splicing in the mouse H-2Kd gene is not necessary for the classical Kd antigen function.

Authors:  M Cochet; W M Kast; A M Kummer; C Transy; C J Melief; P Kourilsky
Journal:  Immunogenetics       Date:  1986       Impact factor: 2.846

2.  Coxsackievirus B-3 myocarditis. Identification of different pathogenic mechanisms in DBA/2 and Balb/c mice.

Authors:  S A Huber; P A Lodge
Journal:  Am J Pathol       Date:  1986-02       Impact factor: 4.307

3.  Cell-mediated immunity induced in mice after vaccination with a protease activation mutant, TR-2, of Sendai virus.

Authors:  M Tashiro; Y Fujii; K Nakamura; M Homma
Journal:  J Virol       Date:  1988-07       Impact factor: 5.103

  3 in total

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