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)

As part of our studies into the role of germinal centers, we investigated whether each de novo generated germinal center (GC) develops from one single GC precursor cell (GCPC, monoclonal development), a few GCPC (oligoclonal development) or from many GCPC (polyclonal development). Thus, lethally (9 Gy) X-irradiated AO (RT1u) rats were reconstituted with 10(8) thoracic duct lymphocytes (TDL) containing mixtures of AO and AO X BN cells in various ratios. The AO TDL were tolerant for AO X BN cells by using TDL from AO----(AO X BN)F1 (RT1u/n) X-irradiation bone marrow chimeras. To induce GC formation in the spleen of TDL-reconstituted rats, animals were i.v. injected with 10(9) sheep red blood cells. Five days after reconstitution and antigenic challenge spleens were taken for analysis of cellular make up of de novo generated GC. Spleen sections were immunohistochemically stained with monoclonal antibody F17-23-2, recognizing major histocompatibility complex class II antigens of the RT1n haplotype but not the RT1u haplotype, to discriminate between B cells of AO and AO X BN origin. Analysis of the GC in spleens of rats reconstituted with a mixture of AO and AO X BN TDL revealed three types of GC: GC entirely composed of AO cells, GC entirely composed of AO X BN cells and GC containing a mixture of both. The relative frequencies of these three types of GC indicated that in our experimental system, de novo GC developed oligoclonally from one to three GCPC. These data strongly suggest that GC are sites of antigen-driven expansion of peripheral B cells to very large clones.
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PMID:Germinal centers develop oligoclonally. 330 68

CD4C/human immunodeficiency virus (HIV) transgenic mice develop an AIDS-like disease. We used this model to study the effects of HIV-1 on dendritic cells (DC). We found a progressive decrease in total DC numbers in the lymph nodes, with a significant accumulation of CD11b(Hi) DC. In the thymus, the recovery of transgenic CD8alpha(+) DC had a tendency to be lower. Spleen DC were augmented in the marginal zone. Transgenic DC showed a decreased capacity to present antigen in vitro, consistent with their reduced major histocompatibility complex class II expression and impaired maturation profile. The accumulation of immature DC may contribute to disease and may reflect an adaptive advantage for the virus by favoring its replication and preventing the generation of fully functional antiviral responses.
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PMID:The AIDS-like disease of CD4C/human immunodeficiency virus transgenic mice is associated with accumulation of immature CD11bHi dendritic cells. 1455 58

Immune control of the protozoan parasite Trypanosoma cruzi requires the activation of both CD4+ and CD8+ T cells. We recently identified two T. cruzi trans-sialidase peptides that are targets of approximately 30% of all CD8+ T cells during acute T. cruzi infection in mice. To determine whether CD4+ T cells are required for generation of these dominant CD8+ T-cell responses, major histocompatibility complex class II (MHC II)-deficient mice were infected with the Brazil strain of T. cruzi and examined for the generation of antigen-specific CD8+ T cells. Strong trans-sialidase TSKB18- and TSKB20-specific CD8+ T-cell responses were generated in both the presence and the absence of CD4+ help. However, the magnitudes of the immunodominant TSKB20-specific CD8+ T-cell responses detectable using class I MHC-peptide tetramers were consistently lower in the blood and spleens of MHC II-deficient mice. Spleen cells from infected MHC II-deficient mice produced gamma interferon after in vitro stimulation with T. cruzi peptides at levels similar to those in wild-type mice, and MHC II-deficient mice displayed strong T. cruzi peptide-specific cytotoxic T-lymphocyte activity in vivo. Thus, primary CD8+ T-cell responses in experimental T. cruzi infection are generated in the absence of CD4+ T cells, providing further evidence that T. cruzi directly activates and licenses antigen-presenting cells. Nevertheless, unhelped CD8+ T cells in T. cruzi-infected mice fail to reach the frequencies achieved in the presence of CD4 T-cell help and are unable to prevent acute-phase death of these mice.
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PMID:Limited role for CD4+ T-cell help in the initial priming of Trypanosoma cruzi-specific CD8+ T cells. 1704 5