Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Irradiated CBA/J mice transplanted with H-2 compatible, minor histocompatibility disparate B10.BR bone marrow develop graft-versus-host disease (GVHD) if mature T lymphocytes are added to the marrow inoculum. In the setting of mild GVHD (receiving 10(4) or 10(5) T cells), by phenotypic analysis, lymphoid reconstitution occurs normally within 4 to 6 wk but there is a profound deficiency in the ability of splenic lymphocytes to respond to polyclonal activators such as LPS and Con A. This unresponsiveness is attributable to active suppression mediated by cells that express Thy-1 and can be removed with leucine methyl ester treatment. Thus, splenocytes from mice with GVHD suppress responses of normal T and B lymphocytes. Moreover, depletion of these suppressor cells restores normal function to splenocytes from mice with GVHD, and B cells isolated from these mice respond normally to T-dependent and -independent stimulation. Finally, IFN-gamma plays an important role in this suppression, because a neutralizing anti-IFN-gamma mAb significantly removes suppression of normal cells and restores functional responses of lymphocytes from mice with GVHD. These results provide insights into the mechanisms of immunodeficiency associated with GVHD, and suggest novel strategies for possible therapies for this disorder.
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PMID:Immunodeficiency in graft-versus-host disease. I. Mechanism of immune suppression. 312 5

Circulating PBMC of healthy subjects possess an in vitro natural antibacterial (NA) against enteropathogenic bacteria, including Salmonella species. The effector cell of NA activity is a CD: 4+, 8-, Leu-8/TQ-1+ T lymphocyte acting against bacteria via cytophylic IgA in a mechanism similar to antibody-dependent cellular activity. Because AIDS is a profound immunodeficiency caused by HIV involving primarily CD4 lymphocytes and in particular the Leu-8/TQ-1 subset, it was of interest to assess NA activity of HIV+ subjects at various stages of the disease. Results indicate that NA activity against Salmonella typhi and Salmonella paratyphi C is significantly decreased in AIDS as well as in lymphadenopathy syndrome patients. Furthermore, sera containing IgA against salmonellae were not able to arm PBMC from HIV+ patients. The humoral response against S. typhi-LPS was also greatly decreased after HIV infection, in contrast to the known hypergammaglobulinemia seen in these subjects. Defective NA activity might contribute to the increased incidence of salmonellosis observed in AIDS.
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PMID:Impairment of in vitro natural antibacterial activity in HIV-infected patients. 326 64

Our studies have revealed that patients with Cystic Fibrosis CF who are infected with P. aeruginosa have grossly elevated serum levels of IgG antibodies to the opsonic immunodeterminant, type-specific LPS. Second, this elevation is distributed among all four IgG subclasses, with a significant shift towards IgG3. Third, sera from colonized CF patients shows diminished opsonic capacity, although complement dependent human neutrophil phagocytosis is not notably impaired. Fourth, functional polyclonal or monoclonal antibody opsonins exhibit prozone inhibition of phagocytosis at high concentrations. Fifth, sera from uninfected CF patients have lower levels and proportions of IgG2 antibodies to P. aeruginosa LPS, and higher levels and proportions of IgG4 antibodies, than normal controls. Finally, levels of IgG4 antibodies, but not IgG1, 2, or 3, correlate inversely with opsonic capacity. We therefore make several speculations. High levels of IgG4 antibodies to opsonic immunodeterminants may inhibit normal pulmonary clearance of P. aeruginosa by alveolar macrophages in vivo. Second, high levels of opsonic antibodies may also contribute to the problem in vivo by the phenomenon of prozone inhibition. Third, reduced levels of IgG2 antibodies in uninfected CF patients raises the intriguing possibility of an wider polysaccharide antigen-related isotype-restricted immunodeficiency, with an attempted compensatory shift to IgG4 doomed to failure.
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PMID:The role of IgG subclass antibodies in chronic infection: the case of cystic fibrosis. 336 9

DBA/2Ha mice have an X-chromosome-linked immunodeficiency and lack the receptor to a TRF (T cell replacing factor) on a subpopulation of B cells. Their immunodeficiency is considered to resemble that of CBA/N, another X-chromosome-linked immunodeficiency. To facilitate direct comparisons of the two immunodeficiencies and to study the in vivo manifestations of DBA/2Ha immunodeficiency, we measured phenotypes and functions of B cells of DBA/2Ha mice. We found that the expression of sIgM among B cells is normal in DBA/2Ha mice, heterozygous females equally express both affected and normal B cell subpopulations, and DBA/2Ha mice respond well to a TI-2 antigen (TNP-Ficoll) and a polyclonal activator (LPS). Unlike CBA/N, DBA/2Ha mice demonstrate very little in vivo immunodeficiencies.
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PMID:Study of the DBA/2Ha immunodeficiency: X-chromosome mosaicism and in vivo immunoresponses. 349 86

The CD4 molecule, which is known to play an important role in the susceptibility of T lymphocytes to infection by the human immunodeficiency virus (HIV), is also expressed in small amounts on the surface of monocytes. Since monocytes can also be infected by the virus, we investigated peripheral blood monocytes of patients with the acquired immunodeficiency syndrome (AIDS), AIDS-related complex (ARC), and HIV seropositive and seronegative haemophiliacs without symptoms for the expression of the CD4 molecule and for other functionally important surface molecules such as CD11 (C3bi receptor), transferrin receptor, Fc receptor, and the three major histocompatibility complex (MHC) class II antigens HLA-DP, HLA-DR, and HLA-DQ. With immunofluorescence staining and flow cytometry no difference was found between patients and controls for the expression of the CD4 molecule and for the other antigens as assessed by the percentage of positive staining and the specific fluorescence intensity in a double marker analysis. The percentage of CD4+ monocytes was found to be 59.2 +/- 14.4% for 16 patients with AIDS and 52.9 +/- 12.8% for 12 healthy controls. Similar to our results on phenotype, we found no significant difference with respect to the production of tumour necrosis factor (TNF), in that monocytes of AIDS and ARC patients showed an increase in TNF secretion after stimulation with LPS comparable to controls.
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PMID:Monocyte phenotype and function in patients with the acquired immunodeficiency syndrome (AIDS) and AIDS-related disorders. 368 87

The incidence of infections caused by gram-negative bacteria is increased in patients with multiple myeloma due to secondary humoral immunodeficiency. In order to diagnose patients with increased susceptibility to gram-negative infections, serum antibodies against common determinants of lipopolysaccharides (lipid A and core-polysaccharide) were determined by a rapid enzyme-linked immunosorbent assay (ELISA). It was possible to define a group of patients at high risk of contracting gram-negative infections using this test. Intravenous IgG preparations used as a substitute were shown to contain antibodies against these common antigens. However, it is suggested that the clinically recognized efficacy of these preparations could be due to their containing anti-LPS antibodies.
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PMID:Serum antibodies against common antigens of bacterial lipopolysaccharides in healthy adults and in patients with multiple myeloma. 403 Jan 7

CBA/N mice, which possess an X-linked immunodeficiency (xid), produce a convincing antibody response to lipopolysaccharide derived from Escherichia coli 0113 (LPS 0113), a thymus-independent antigen. The antibody response produced was shown to be specific for the O-polysaccharide moiety of LPS 0113, rather than lipid A or lipid-A-associated protein. The relevance of this finding to the nature of the genetic defect of xid-mice is discussed.
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PMID:Antibody response of immunodeficient (xid) CBA/N mice to Escherichia coli 0113 lipopolysaccharide, a thymus-independent antigen. 618 86

C57BL/10ScCr mice are low responders to the alpha 1-6 epitope of dextran B512, although other C57BL mice are high responders. Both thymus-independent and thymus-dependent forms of dextran failed to induce an immune response in C57BL/10ScCr mice, but dextran functioned as a good carrier for antihapten responses in this strain. Dextran is a potent polyclonal B cell activator for cells from C57BL/10ScCr mice, although such cells are not activated by LPS. The C57BL/10ScCr mice possess the Igh-V gene coding for antibodies against dextran and the antidextran antibodies induced in (A X C57BL/10ScCr)F1 hybrids share an idiotype with antidextran antibodies produced in C57BL/10 mice. Bone marrow cells from C57BL/10ScCr mice do not respond to dextran when transferred into lethally irradiated C57BL/10 mice and C57BL/10 cells transferred into C57BL/10ScCr mice give a strong antidextran response. Thus, B cells having both the Igh-V gene coding for antibodies against dextran and activation receptors for dextran cannot be activated into antibody synthesis against any form of this immunogen. This determinant specific immunodeficiency suggests the existence of as yet unknown regulatory influences on Igh-V gene expression or B cell activation.
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PMID:Mechanism of unresponsiveness to the alpha 1-6 epitope of dextran B512 in a C57BL substrain. 619 Sep 81

Parotid protein (extracted from bovine parotid gland), one parotid subunit, and the active fragment (FrAA-1) induced polyclonal IgM, IgG, and IgA antibody production in murine spleen cells in vivo and in vitro. The parotid subunit also elicited polyclonal IgM antibody responses in immune defective CBA/N and LPS nonresponder C3H/HeJ mouse. When one carbohydrate residue in the subunit was removed by treatment with mixed galactosidase, the ability to generate nonspecific responses was markedly reduced. In human peripheral lymphocytes, the parotid subunit and FrAA-1 induced considerable polyclonal IgM antibody production. The subunit was not toxic to human lymphocytes. Therefore, it seems possible that parotid protein could be applied to immunopharmacological therapy for conditions such as immunodeficiency.
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PMID:Polyclonal antibody production induced by parotid protein and its active glycopeptide in mouse and human lymphocytes. 688 80

CBA/N mice and F1 crosses of CBA/N X BALB/c with the CBA/N phenotype respond to immunization with PC-LPS with a PC-specific and an anti-bridge antibody production. The PC-specific response in defective CBA/N and NBF1 is devoid of the IgG3 subclass and is not T15 idiotype dominant, whereas normal BALB/c and nondefective NBF1 mice express the T15 dominantly in their anti-PC-LPS response. By the criteria of responsiveness to PC-LPS only and the absence of dominant T15 expression, the precursors in defective NBF1 mice for TI-1 antigen PC-LPS can be characterized as being immature B cells similar to those found in neonatal livers of normal BALB/c or in spleens of chronically idiotype suppressed BALB/c mice. This analogy suggests that the developmental defect in CBA/N mice becomes active during the maturation process before selection for clonal dominance occurs and specialization of precursors for the preferred expression of the IgG3 subclass is completed. Alterations in the T cell compartment may contribute to the immature nature of B cells in the sex-linked immunodeficiency of CBA/N mice.
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PMID:Immune response to phosphorylcholine. VIII. The response CBA/N mice to PC-LPS. 721 66


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