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

We have been studying the mitogen hyporesponsiveness and immunosuppression induced in chronic murine graft-vs.-host disease (GVHD) induced across minor histocompatibility (MiHA) barriers. In this system, donor and recipient mice are major histocompatibility complex- and mls-identical, and are nonreactive in primary mixed leukocyte reactions. Spleen cells from B10.D2 (H-2d, mls b) mice were injected into irradiated (600 rad) BALB/c (H-2d, mls b) recipients. Recipient spleen cells are hyporesponsive to mitogens, and contain natural suppressor (NS) cells. We investigated the cellular requirements for both the in vivo induction and the in vitro expression of this GVH suppression. T cells are required in the graft, but they are not sufficient to induce suppression, and a non-T cell population is also required for maximum induction in vivo. T cells are also required for the maximum expression of NS cell suppressive ability in vitro. Early in the course of GVH, the suppressor cells are able to suppress the Con A and LPS response of all mouse strains tested (except for the relative difficulty in suppressing the B10.D2 LPS response). Later, they become almost completely unable to suppress the B10.D2 LPS response; while still being able to suppress the Con A and LPS response of all other strains tested (including the B10.D2 Con A response). This inability to suppress a B10.D2 LPS response can be brought back to almost complete suppression by the addition of concanavalin A supernatant (CAS). We present a hypothesis to explain what may be a common mechanism for GVH-induced suppression, total lymphoid irradiation-induced suppression, and neonatal tolerance. These situations all include rapidly proliferating lymphohematopoietic stem cell populations, and also have large numbers of NS cells. NS cells can suppress proliferating lymphoid populations, and their development and activity are greatly enhanced by T cell signals such as are supplied by donor T cells in chronic GVHD. Thus, NS cells may feed back on and downregulate self-reactive T cells or T cells responding to introduced foreign antigens.
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PMID:Synergism between T and non-T cells in the in vivo induction and in vitro expression of graft-vs.-host disease-induced natural suppressor cells. 316 77

Cultures of synovial cells from normal CBA mice were established after collagenase treatment of synovial tissue collected from the knee joint. Morphological studies using light and electron microscopy have shown that confluent monolayers are composed of 90% triangular or stellate dendritic cells with numerous microvilli and 5% secreting cells containing many dense granules. Less than 5% contaminating cells, such as fibroblasts or macrophages, are present. The class I and class II antigens of the major histocompatibility complex, detected by indirect immunofluorescence or complement-dependent cytotoxicity, are expressed on the cell surface of normal CBA synovial monolayers. Functional Ia antigens borne by synoviocytes are evidenced by the proliferative responses they elicit from syngeneic (or allogeneic) spleen cells after a 3-day co-culture. Similarly, monolayers of Ia+ synovial cells were obtained from both MRL/lpr mice, which spontaneously develop an autoimmune syndrome, and the control MRL/n mice. Spleen cells from young MRL/lpr exhibited significantly higher levels of blastogenesis in syngeneic co-cultures than those from MRL/n mice. Conversely, with advancing age the syngeneic proliferative responses declined minimally for MRL/lpr mice and were unchanged for MRL/n mice. These findings suggest that Ia+ synovial cells can effectively interact with syngeneic lymphocytes and may initiate autoimmune reactivity.
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PMID:Functional role in self reactivity for Ia antigens on murine synovial cells. 349 45

The function of a transgenic Dd class I molecule in the induction of immunologic tolerance to major histocompatibility complex antigens and in directing major histocompatibility complex restriction in C57BL/6 mice were investigated. All of the transgenic Dd mouse strains were found to be tolerant for the Dd antigen. Spleen cells from transgenic mice were immunocompetent but consistently failed to generate an anti-Dd cytotoxic T lymphocyte response in vitro, and skin grafts between transgenic Dd mice were not rejected. These data suggests that the Dd antigen was recognized as a self molecule. In addition, the transgenic Dd mice generated antigen-specific Dd-restricted cytotoxic T lymphocyte, indicating that the Dd antigen also functioned as a restriction element for antigen recognition. These observations demonstrate the usefulness of the transgenic mouse system for studying class I antigen expression and function.
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PMID:A transgenic class I antigen is recognized as self and functions as a restriction element. 350 Feb 31

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

The existence of T cells specific for soluble antigens in association with unique F(1) or recombinant major histocompatibility complex (MHC) gene products was first postulated from studies on the proliferative response of whole T cell populations to the antigen poly(Glu(55)Lys(36)Phe(9))(n) (GLphi). In this paper we use the newly developed technology of T lymphocyte cloning to establish unequivocally the existence of such cells specific for GLphi and to generalize their existence by showing that F(1)- specific cells can be isolated from T cell populations primed to poly(Glu(60)Ala(30)Tyr(10))(n) (GAT) where such clones represent only a minor subpopulation of cells. Gl.4b-primed B10.A(5R) and GAT-primed (B10.A x B10)F(1) lymph node T cells were cloned in soft agar, and the colonies that developed were picked and expanded in liquid culture. The GLphi-specific T cells were then recloned under conditions of high-plating efficiency to ensure that the final colonies originated from single cells. T cells from such rigorously cloned populations responded to stimulation with GILphi but only in the presence of nonimmune, irradiated spleen cells bearing (B10.A x B10)F(1) or the syngeneic B 10.A(5R) recombinant MHC haplotype. Spleen cells from either the B10 or B 10.A parental strains failed to support a proliferative response, even when added together. (B10 x B10.D2)F(1) and (B10 x B10.RIII)F(1) spleen cells also supported a proliferative response but (B10 x B10.Q)F(1) and (B10 X B10.S)F(1) spleen cells did not. These results suggested that the T cell clones were specific for GL[phi} in association with the beta(AE)(b)-alpha(E) (k,d,r,) Ia molecule and that recognition required both gene products to be expressed in the same antigen-presenting cells. Support for this interpretation was obtained from inhibition experiments using the monoclonal antibody Y-17 specific for a determinant on the beta(AE)(b)-alphaE Ia molecule. Y-17 completely inhibited the proliferative response of a GLphi-specific clone but had no effect on the response of either a PPD-specific or GAT-specific clone, both of which required the beta(A)-alpha(A) Ia molecule as their restriction element. No evidence could be found for the involvement of suppressor T cells in this inhibition. We therefore conclude that the phenomenon of F(1)-restricted recognition by proliferating T cells results from the presence of antigen- specific clones that must recognize unique F(1) or recombinant Ia molecules on the surface of antigen-presenting cells in addition to antigen in order to be stimulated.
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PMID:Antigen-specific T cell clones restricted to unique F1 major histocompatibility complex determinants. Inhibition of proliferation with monoclonal anti-Ia antibody. 616 4

A potent mitogen for T lymphocytes of various species has recently been isolated from the supernatant of cultured Mycoplasma arthritidis organisms (MAS). In the mouse, reactivity to this mitogen has been observed to be controlled by the I-E subregion of the major histocompatibility complex. We have analysed the responses of spleen cells from several inbred rat strains covering practically all known haplotypes of the major histocompatibility complex of the rat (RT1). Unlike in the mouse, all of these responded well to MAS, except for the BN rat strain, which is a low responder to all T-cell mitogens, including phytohaemagglutinin and concanavalin A. This unresponsiveness, however, appeared to be unrelated to the RT1 haplotype, since LEW.1N rats carrying the same RT1n haplotype as BN animals responded well. Mice of the strain C57BL/6 are non-responders to MAS, but--as previously shown--their spleen cell responses can be reconstituted by the addition of 2-mercaptoethanol. No such reconstitution was observed for the low responsiveness of BN rat spleen cells. Stimulation with MAS induced high titres of interferon (presumably gamma interferon) in spleen cells from all rat strains tested. Spleen cells from BN rats produced lower interferon activities than those from other strains.
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PMID:Lymphoproliferative responses of spleen cells of inbred rat strains to Mycoplasma arthritidis mitogen. 620 89

The major histocompatibility complex of the rat (RTl) is composed of at least five subregions. They are RTl-A,B,C,D and E regions. RTl-A,E and RTl-B,D regions encode class I and class II alloantigens, respectively. The RTl-C region encodes antigens which are similar to class I alloantigens and they are the homologue of mouse Qa-Tla antigens. A monoclonal antibody (X81-5C9) was produced against a rat B-cell leukemia, KNL-14. The KNL-14 cells were injected to a congenic rat, WKA. 1A(ACI). Spleen cells taken from the congenic rat were hybridized with mouse myeloma cell line P3.X63.Ag8.653. The monoclonal antibody lysed over 80% of nylon wool (N. W) adherent cells of lymph nodes, 25-30% of unseparated lymph node cells and/or spleen cells, and approximately 15-20% of peripheral blood lymphocytes of WKAH strain of rats. Only a portion (30-40%) of N. W. adherent cells of the peripheral blood lymphocytes was killed. Bone marrow cells, thymus cells and N. W. nonadherent cells were not lysed by the antibody. Macrophages, fetus, thymus and kidney homogenates could absorb the reactivity, whereas RBC, epidermal cells, brain, liver, testis could not absorb the cytotoxicity. A survey for the strain distribution of the antigen disclosed positive strains such as WKAH, W/Hok, LEJ, WKA. 1J (LEJ), ALB, WKA. 1B (ALB), BUF, BN, LEW, F344, W. 1L (F344) and KYN rats. The negative strains were NIG-III, WF, WKA. 1U WF), SDJ, W. 1U (SDJ), TO, W. 1T(TO), ACI, WKA. 1A(ACI), BDIX, WKA. 1DV1 (BDIX) and PVG/c rats. Immunochemically, the antibody precipitated antigens that gave two major bands on the SDS-PAGE. The heavy chain has an apparent molecular weight of 30 KD, which shifted to 33 KD under reducing conditions. The light chain has an apparent molecular weight of 12 KD. From these data a monoclonal antibody X81-5C9 is considered to detect a rat MHC (RTl) gene product which is different from the classic class I or class II cell surface antigens. It may be one of RTl-C antigens expressed mainly on B-cells. The characteristic feature of rat RTl-C antigens were discussed in relation to mouse Qa-Tla antigens.
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PMID:[A new B-cell alloantigen of the rat]. 623 70

Adoptive transfer of ectromelia virus meningitis was most efficient when donor-immune spleen cells and recipients were compatible in the K region of the H-2 gene complex. Weak responses could be obtained with H-2D region compatibility, but none occurred with H-2I region compatibility. Spleen cells used in adoptive transfers and cells found in cerebrospinal fluid from infected mice were found to have identical H-2-imposed restriction in their in vitro cytotoxic activity. This suggests a significant role for the major histocompatibility complex in the generation of virus-specific T lymphocytes and the recognition of virus-infected tissue in the central nervous system by these cells.
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PMID:The role of the major histocompatibility complex in the adoptive transfer of ectromelia virus meningitis. 627 37

Spleen and lymph node cells of BALB/c mice, previously immunized with chicken thymic or bursa cells, were fused with Sp2/0-Ag14 mouse myeloma cells. Hybridomas from two fusions were selected on the basis of reactivity of their secreted antibodies towards thymic or bursal tissues in an indirect immunofluorescence assay. Four monoclonal antibodies reacting with different cell surface proteins of chicken lymphocytes were characterized, as follows. One antibody (IgM X.14) reacted only with cortical thymocytes, and precipitated material of apparent molecular weight (AMW) 65,000 (65 kD), 125 kD, and 180 kD from these cells. A second antibody (IgGl L.17) reacted with both bursa- and thymus-derived lymphocytes, but with different high molecular weight glycoproteins (AMWs 210 kD and 180 kD, respectively) on the two cell types. These proteins may be homologues of the previously described mouse B-220 and T-200 antigens. A third antibody (IgGl L.22) reacted with a protein of AMW 70 kD present on bursa-derived cells of some, but not all, chicken strains. Genetic analysis suggested that the presence of this protein was controlled by a single gene not closely linked to the major histocompatibility complex. A fourth antibody (IgG2b L.43) reacted with bursa-derived cells, macrophages and fibroblasts, but not with thymus-derived lymphocytes. L.43 precipitated material of AMW 23 kD from bursal cells.
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PMID:Monoclonal antibodies against chicken lymphocyte surface antigens. 633 57

Thymectomy of very young Xenopus larvae abrogated in vitro proliferative responses to phytohemagglutinin (PHA) and allogeneic leukocytes. Thymectomized (Txd) frogs, however, still rejected first-set skin allografts chronically and second-set grafts (but not third-party grafts) more rapidly. The specific second-set rejection reaction by Txd frogs was transferable in vivo to secondary Txd hosts (with major histocompatibility complex identical to the cell donor) by the subcutaneous injection of a mixture of splenic and peripheral blood leukocytes. Spleen cells used in this adoptive transfer experiment (i.e., immune cells) were responsive to allogeneic cells from the original donor strain as well as from unrelated donors in mixed leukocyte culture in vitro but were still unreactive to PHA. The results are consistent with an extrathymic pathway of alloreactive cell differentiation in this species, although the physiological significance of such a pathway is not clear.
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PMID:Specific in vivo and nonspecific in vitro alloreactivities of adult frogs (Xenopus laevis) that were thymectomized during early larval life. 634 94


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