Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The H-2Ld allele has been identified by others as the sole Ir gene in the H-2d haplotype for the cytotoxic T lymphocyte (CTL) response to mouse lymphocytic choriomeningitis virus (LCMV). The BALB/c-H-2dm2 (C-H-2dm2) mutant lacks H-2Ld, and thus should be ideal for assessing the contribution of virus-immune CTL to LCM immunopathology. Comparison of the C-H-2dm2 mice with congenic BALB/c mice revealed that there is a delay of about 24 h in the onset of severe inflammatory process and symptoms in the mutant strain, but the absence of H-2Ld did not prevent the later development of fatal disease in mice injected intracerebrally (i.c.) with neurotropic LCMV. This could indicate that virus-immune CTL are not the major mediators of clinical LCM. Spleen cells from LCMV-primed BALB/c mice did not show CTL activity for LCMV-infected C3H.OH, C-H-2dm2, or (CBA X C-H-2dm2)F1 target cells. However, immune lymphocytes from both the mutant and the F1 strains lyse virus-infected BALB/c cells. Furthermore, B10.HTG and, in some experiments, B10.A(5R) mice generated CTL lytic for LCMV-infected BALB/c, C-H-2dm2, and (CBA X C-H-2dm2)F1 macrophages. Apparently H-2Ld is immunodominant in the H-2d-restricted response to LCMV. However, in the absence of H-2Ld, it seems that H-2Kd and, to a lesser extent, H-2Dd also serve as Ir genes for the CTL response in this infection. Even so, the absence of the H-2Ld-restricting element results in a disease process which is either delayed in onset or less severe.
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PMID:Consequences of a single Ir-gene defect for the pathogenesis of lymphocytic choriomeningitis. 387 59

Spleen T lymphocytes from mice undergoing acute infection with lymphocytic choriomeningitis virus (LCM virus) were negatively selected by treatment with anti-Lyt or anti-L3T4 antibodies and complement. The subsets thus obtained were tested for their potential to lyse LCM virus-infected target cells in vitro and to confer on infected syngeneic recipients the ability to eliminate virus rapidly from their spleens. Both capacities were found to be associated with Lyt-1-2+, L3T4- cells. Previous studies had shown that LCM virus-specific cytotoxicity in vitro as well as reduction of replication of LCM virus in the adoptively immunized mouse requires compatibility at K and/or D of the major histocompatibility complex, and we conclude that clearance of LCM virus from the mouse's spleen is mediated by the subset of T lymphocytes that is functionally characterized as cytotoxic/suppressive.
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PMID:Mechanism of recovery from acute virus infection. III. Subclass of T lymphocytes mediating clearance of lymphocytic choriomeningitis virus from the spleens of mice. 387 30