Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q00604 (X-linked)
 16,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CBA/N mice have an X-linked immune defect in B lymphocyte function which leads to their inability to respond to several thymus-independent antigens. We report here that these mice and immunologically defective F1 male (CBA/N X DBA/2N) mice can respond to Brucella abortus and to 2,4,6-trinitrophenyl derivatives of Brucella abortus (TNP-BA). These responses can be obtained in vivo and in vitro and are thymus-independent by the criteria that (a) they can be transferred to irradiated recipients by bone marrow cells and anti-Thy-1.2 and complement-treated spleen cells; (b) that nu/nu BALB/c spleen cells respond to TNP-BA in vitro; and (c) that anti-Thy-1.2 and complement-treated (CBA/N X DBA/2N)F1 male spleen cells respond to TNP-BA in vitro. B. abortus and TNP-BA are poor polyclonal B cell activators (PBA) and poor B cell mitogens, unlike lipopolysaccharide which is both a powerful PBA and B cell mitogen. These results therefore indicate that mice with the CBA/N B cell defect can respond to some thymus-independent antigens, namely TNP-BA, and as shown previously, TNP-LPS, although not to other thymus-independent antigens. This, in turn, suggests that thymus-independent antigens may be subdivided on the basis of their ability or inability to stimulate responses by CBA/N B lymphocytes.
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PMID:T-independent responses in B cell-defective CBA/N mice to Brucella abortus and to trinitrophenyl (TNP) conjugates of Brucella abortus. 9 20

The effect of age on the mitogenic and antigenic responsiveness of B cells is examined in spleen cell cultures of CBA/N and (CBA/N X DBA/2) F1 mice. Spleen cells from young male F1 mice (4- to 6-wk old) show lower mitogenic responses to lipopolysaccharide, a lower frequency of sheep erythrocytes (SRBC)-reactive B-cell precursors, and a lower percentage of Ig-bearing cells than age-matched female F1 mice. The expression of all three functions were found to increase with the age of the F1 male mice. Whereas male F1 mice at 60 wk of age showed an equivalent percentage of Ig-bearing spleen cells and a similar mitogenic responsiveness to LPS when compared to adult female F1 mice, the frequency of SRBC-reactive B-cell precursors remained threefold lower. These findings reveal that there is a slower maturation of B cells in mice expressing the X-linked defect and suggests that the defect has differential effects on the mechanisms of antigen and mitogen activation of B cells.
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PMID:B-cell differentiation in the CBA/N mouse. I. Slower maturation of mitogen and antigen-responsive B cells in mice expressing an X-linked defect. 31 94

Immunization of congenitally athymic (nu/nu) and adult thymectomized, irradiated bone marrow, reconstituted (TxBm) mice with DNP5-thymosin (dinitrophenylated-bovine thymosin fraction 5) was found to elcit IgM and IgG anti-DNP plaque-forming cells in these animals. Further studies indicated that this response was antigen specific and not due to polyclonal activation. Since the hormonal properties of the thymosin were retained following linkage with hapten and DNP-thymosin was immunogenic in CBA/N and CBA/N female X DBA/2 male)F1 male mice, animals previously shown to have an X-linked inability to respond to thymus-independent antigens, it was concluded that DNP-thymosin functions both as a hormone and as a T-dependent antigen in eliciting an immune response in nu/nu and TxBm mice. Additional support for this conclusion was provided by the demonstration that DNP-thymosin could specifically prime for and elicit an anamnestic response in nu/nu mice. These results indicate that further investigation of the immune activities of DNP-thymosin may provide valuable insight in characterizing the maturation of helper T cells and their subsequent interaction with B cells.
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PMID:Thymic-dependent anti-hapten response in congenitally athymic (nude) mice immunized with DNP-thymosin. 33 78

Investigators from this laboratory have been studying sex hormones in normal and autoimmune mice for the past 10 years. We have found that immune responses to DNa are influenced by sex hormones. Androgens reduce and estrogens increase both spontaneous and immunization-induced antibodies to single-stranded DNA in NZB X NZW, NZB X C3H, NZB X CBA, NZB X DBA mice. Treatment of female NZB/W mice with testosterone or 5 alpha dihydrotestosterone retards the progress of autoimmunity. Castration is not necessary for this effect. In contrast, danazol has no favorable effect on the disease process. Estrogens cause a marked acceleration of autoimmunity and a reduction in thymus weight. During the course of these studies, we found that a number of problems or variables arise in studying sex hormone effects, including: 1) X-linked genes, 2) metabolism of testosterone to estrogens, 3) dose of hormone, 4) age at which administration is initiated, 5) differential effects of sex hormones on different autoantibodies and various immune responses.
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PMID:Approach to the study of the role of sex hormones in autoimmunity. 50 71

The linkage relationships of the lethal gene blind (Bld) in the mouse were investigated. The gene is located on chromosome 15, between uw and bt. The distance uw--Bld is 28.2 +/- 5.1 cM: Bld--bt is 14.9 +/- 2.7 cM: and Bld--Ca is 24.6 +/- 2.6 cM. Incomplete penetrance and/or reduced viability of Bld/+ animals was found when blind animals were crossed to several strains, but the cross female DBA/2J X male blind yielded complete penetrance and specificity. Evidence is presented for the presence of X-linked modifiers affecting the penetrance and possible increased viability of Bld in strain DBA.
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PMID:The genetics of blind--a lethal factor in mice. 67 Jun 79

Spleen cells from CBA/N mice with an X-linked B cell defect were examined for their ability to form antibody in vitro after stimulation with the T-independent antigen TNP-LPS. In contradistinction to their failure to respond to some conventional T-independent antigens such as type III pneumococcal polysaccharide or DNP-AECM-Ficoll, spleen cells from (CBA/N X DBA/2)F1 male mice were able to make a specific anti-TNP PFC response after culture with TNP-LPS. Their response differed from that of phenotypically normal (CBA/N X DBA/2)F1 female littermate spleen cells in that more TNP-LPS was required to elicit the peak anti-TNP response and the anti-TNP antibody secreted by F1 male cells was of lower avidity than that of F1 female cells. The polyclonal antibody response to unsubstituted LPS did not differ substantially between normal and defective B cells. Tnymus-derived cells were not required for the TNP-LPS response by either F1 male or female cells. We conclude that CBA/NB cells can respond to certain T-independent antigens that are able either to induce a very strong activating signal upon ligand-surface receptor interaction and/or to stimulate immature B cells (with a characteristic high surfact immunoglobulin profile) which fail to respond to antigens like DNP-AECM-Ficoll.
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PMID:In vitro responses of CBA/N mice: spleen cells of mice with an X-linked defect that precludes immune responses to several thymus-independent antigens can respond to TNP-lipopolysaccharide. 78 72

The mechanisms underlying the X-linked thymus-independent (B) lymphocyte functional defect in the CBA/N (CN) mice and their F1 progeny were studied. Immune defective mice were unable to respond to the T-independent antigen 2,4-dinitrophenyl-lysyl-derivative of Ficoll (DNP-lys-Ficoll) but were able to form antibody against the highly cross-reactive hapten (trinitrophenyl) when it was coupled to an erythrocyte carrier. Immune defective CN X DBA/2N (DN) F1 male mice, which do not normally respond to T-independent antigens, were able to respond to both polyribosinic-polyribocytidylic acid and DNP-lys-Ficoll after the administration of CN X DN F1 female spleen cells even if these cells had been depleted of T lymphocytes. In addition, it was shown that the inability of the CN mice and their F1 progeny to respond to T-independent antigens was not due to an intrinsic abnormality of their microenvironment or the suppressive actions of a T lymphocyte. Our data present evidence that the X-linked defect in the CN mice is due to an intrinsic defect in B-lymphocyte development.
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PMID:X-linked B-lymphocyte immune defect in CBA/N mice. II. Studies of the mechanisms underlying the immune defect. 108 Jul 88

X-linked immunodeficient (xid) (CBA/N female x DBA/2 male) F1 male mice, when treated with cyclophosphamide, were much more susceptible to challenge with aerosolized Pseudomonas aeruginosa serotype 11 than were control F1 female littermates. Mortality of F1 males was decreased significantly after intravenous administration of human P. aeruginosa serotype 11 O-specific monoclonal antibody. Antibody treatment reduced bacterial titers in the lungs as well as the severity of Pseudomonas-induced lung histopathology.
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PMID:A human monoclonal antibody that protects mice against Pseudomonas-induced pneumonia. 211 78

Differentiation of B lymphocytes from various peripheral lymph nodes (PLN) of mice was studied in the in vitro and in vivo conditions. Subcutaneous (SC) immunization in the foot pads with thymic independent (TI)-2 antigens such as polyvinyl pyrrolidone (PVP), R36A, and Trinitrophenyl (TNP)-Dextran failed to elicit plaque forming cell (PFC) responses from the draining popliteal and inguinal lymph nodes, whereas the splenic B cells of these animals exhibited good PFC response. Injection of unconjugated Brucella abortus (BA) along with TNP-Dextran was able to induce anti-TNP PFC formation from the draining lymph node B cells. However, PVP + BA or R36A + BA failed to stimulate such antigen specific B cell responses from the lymph nodes. Since TI antigens are metabolized slowly because of their long repeating subunits, we measured antibody responses up to 8 weeks after SC immunization with TNP-Ficoll and failed to observe any anti-TNP IgM PFC in the lymph nodes. TNP-Ficoll, in contrast to TI-1 antigen TNP-BA, did not induce IgG PFC response in the draining lymph node cells. In in vitro cultures, TNP-Ficoll induced the B cell differentiation from mesenteric lymph node (MLN) cells but not from the PLN cells. This activation of MLN B cells with TNP-Ficoll was limited to normal DBA/2J mice and was absent in the MLN cells of X-linked immune defective CBA/N mice. Finally, there was good antibody response from the inguinal and lumbar lymph node cells after an intraperitoneal immunization with TNP-BA but not with TNP-Ficoll.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antibody responses to thymic independent antigens in the peripheral and mesenteric lymph nodes of mice. 212 Dec 16

The Peyer's patches (PP) of X-linked immunodeficient (xid) CBA/N and hemizygous (CBA/N X DBA/2)F1 (CDF1) male mice contain a B cell subpopulation that expresses the Lyb-5 maturational marker and is responsive to type 2 and T cell-dependent antigens in vitro, a B cell phenotype which is absent from the spleens of xid mice. Experiments reported here show that xid spleen B cells co-cultured with B cell-depleted PP cells from xid mice differentiated into specific plaque-forming cells in response to trinitrophenyl-Ficoll (type 2) and sheep erythrocytes (T cell-dependent). Two cell types were involved in this normalization of xid B cell responses. An accessory cell activity present in the PP, but not the spleens, of both CDF1 male (xid) and CDF1 female (normal) mice was required for the response to either the type 2 or T cell-dependent antigens. In the presence of this PP accessory cell, T cells from the PP of either xid or normal mice supported responses to both classes of antigens. In contrast, T cells from the spleens of xid mice did not support the response to trinitrophenyl-Ficoll, although the splenic T cells from normal mice did synergize with PP accessory cells in allowing plaque-forming cell development by xid B cells to this type 2 antigen. The xid PP T cell activity required for the type 2 response by xid B cells was present in the Ly-1+, Lyt-2- subpopulation, and the xid PP accessory cell activity was provided by an enriched population of dendritic accessory cells. These results demonstrate the the lymphoreticular cells comprising the PP microenvironment provide effective support for the differentiation of xid B cells in response to type 2 and T cell-dependent antigens.
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PMID:Immunoregulation in the Peyer's patch microenvironment. Cellular basis for the enhanced responses by the B cells of X-linked immunodeficient CBA/N mice. 295 43


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