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Results for “Immune dysfunction”

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At least 217 records · Page 12Linked to original sources
PubMed1991

Immune dysfunction in mice with plasmacytomas. I. Evidence that transforming growth factor-beta contributes to the altered expression of activation receptors on host B lymphocytes.

Plasmacytoma-bearing mice (PC-mice) develop a polyclonal B cell immunodeficiency syndrome characterized by marked impairment of: a) primary antibody responses and b) proliferative responses to B cell mitogens. The present investigations used two-color flow cytometry to examine B lymphocytes from the spleens and lymph nodes of PC-mice and found decreased surface membrane expression of surface IgM (sIgM), transferrin receptors (TfR) and IgE FcR (CD23), increased expression of class II MHC, but normal expression of B220, Mel-14, Fc gamma RII, and Fc mu R. These changes were not related to the H chain class or the amount of Ig produced by the plasmacytoma. When cultured with IL-4, B lymphocytes from PC-mice increased their expression of sIgM and class II MHC, but not of CD23. Several findings implicate transforming growth factor-beta 1 (TGF-beta 1) in the mechanism that modulates receptor expression on B lymphocytes in PC-mice: a) ascites fluid from PC-mice contains large quantities of TGF-beta 1; b) supernatants of cultured spleen cells from PC mice contain up to eightfold more TGF-beta than is found with normal spleen cells; c) cloned plasmacytoma cells produce TGF-beta in vitro; and d) the abnormal phenotype of B cells from PC-mice, i.e., decreased CD23, sIgM, and TfR, and increased class II MHC, is induced on normal B cells cultured in the presence of TGF-beta 1. Because sIgM, TfR, class II MHC, and CD23 are molecules that play fundamental roles in the activation of normal B cells, their modulation by TGF-beta 1: a) identifies molecular mechanisms that could account for some of the known immunosuppressive properties of TGF-beta 1 and b) implicates TGF-beta in the pathogenesis of the polyclonal B cell immunodeficiency that is characteristic of plasma cell tumors.

Animals↗
PubMed1989

Humoral and cellular immune dysfunction in a patient with Bloom's syndrome and recurrent infections.

Immunological evaluation of a patient with Bloom's syndrome (BS) who suffered from recurrent bacterial and fungal infections, revealed low serum levels of IgG and high levels of IgM accompanied by an elevated proportion of surface membrane IgM positive B-lymphocytes and a decreased proportion of IgG positive B-cells. In vitro IgG secretion was also reduced whereas IgM production was normal. Although proportions of T-cell subsets were normal and proliferative responses to T-cell mitogens were adequate, a defective regulatory T-cell function for the generation of IgG was observed. Natural killer (NK) cell activity against K562 tumor cells was also decreased in this patient. The findings in this patient may suggest a maturation arrest of lymphocytes at an early developmental stage, and this may explain in part the increased susceptibility to infections.

Adolescent↗
PubMed1989

Immune dysfunctions in psychiatric patients.

Alterations in the serum proteins and immunoglobulins have been investigated in the search for the possible etiological causes of schizophrenic patients. The results, so far, have been varied and inconclusive. We assayed serum immunoglobulins, and antinuclear antibody (ANA) titres in 94 randomly selected, recently hospitalized, psychotic patients. A complete physical, neurological, laboratory and electrophysiological examination was conducted on each patient. Systems survey and family, as well as past histories were obtained. Our results indicated that 12 patients had high titres of ANA and none of them had any other clinical evidence of autoimmune disease. This finding did not correlated with age, sex, diagnosis, or duration if illness, but an association with the medications that the patients were receiving, was noted. The elevation in ANA titres seems to be related to use of lithium as well as neuroleptics. Our data suggests that all neuroleptics can produce high ANA titres. Systematic study of this phenomenon and their long-term consequences warrant further exploration.

Adolescent↗
PubMed1988

Effect of lithium carbonate in HIV-infected patients with immune dysfunction.

Ten homosexual men received oral lithium carbonate at doses that maintained their serum lithium concentrations between 0.5 and 1.5 mEq/L. Prior to treatment all patients had HIV isolated from PHA-activated peripheral blood lymphocytes (PBLs) using a quantitative antigen-capture enzyme-linked immunosorbent assay (ELISA) assay for detection, and had an absolute number of CD4 (helper) lymphocytes of less than 300/mm3. Eight of 10 patients developed symptoms of drug toxicity requiring discontinuation of the drug in 7 patients. Two patients completed only 4-5 weeks of lithium therapy, and 5 patients received 7-8 weeks. All patients remained culture positive for HIV during the trial, and viral titers as measured by the antigen capture assay were unchanged or increased. There were no significant changes in the absolute number of CD4 lymphocytes, CD4/CD8 ratio, or phytohemagglutinin (PHA) or tetanus toxoid induced proliferative responses. There was a significant decrease in mixed lymphocyte reaction (MLR). Lithium carbonate demonstrated no immunorestorative or antiviral activity when given in therapeutic doses. Drug toxicity limited therapy in the majority of patients.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Immune dysfunction in primary biliary cirrhosis (PBC): I. Increased sensitivity of PHA stimulated lymphocyte cultures to indomethacin.

A reduced responsiveness of peripheral blood lymphocytes from PBC patients to phytohaemagglutinin (PHA) was observed. Such an alteration may be related either to an intrinsic defect of T cells to proliferate or to a derangement of endogenously secreted mediators with regulatory functions, i.e., prostaglandins (PG). The role of the PG mediated suppressor system in 14 PBC patients and in 12 age and sex matched controls was evaluated. After the addition of indomethacin, the lymphocyte responsiveness to PHA increased in both controls and in PBC patients. However, this increment was statistically significantly only in PBC patients. The addition of PGE1 and PGE2 to PHA stimulated cultures decreased the lymphocyte proliferative activity. No differential sensitivity to PGEs was detectable in lymphocytes from PBC patients. Our data suggest, that, after polyclonal stimulation, mononuclear cells from PBC patient may release increased levels of PGEs which in turn affect the proliferative activity of mitogen activated lymphocytes.

Adult↗