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Biomedical subjects

S Raziuddin

Publications and source records attributed to S Raziuddin.

At least 37 records · Page 2Linked to original sources
PubMed1993

Cytokine production by helper T cell populations from the synovial fluid and blood in patients with rheumatoid arthritis.

OBJECTIVE: Our study was undertaken to determine the phenotypic changes and cytokine production from the synovial fluid (SF) and blood of patients with rheumatoid arthritis (RA). METHODS: Blood and SF purified T cells were stained with monoclonal antibodies using standard, indirect immunofluorescence technique for the determination of T cell receptor (TcR) TcR alpha beta and TcR gamma delta antigen expressions, CD25, CD38, CD71, HLA-DR activation antigens, and for percentage distribution of CD4+CD29+ and CD4+CD45RA+ subsets. The production of interleukin 2 (IL-2), IL-4 and IL-6 by various T cell compartments was determined by the bioassay or enzyme linked immunosorbent assay methods. RESULTS: Highly elevated percentage of CD3+TcR gamma delta and CD4+CD29+ T cell subsets were detected in SF and blood of RA. The CD4+CD29+ T cell subsets produced elevated levels of IL-4 and IL-6 but deficient levels of IL-2. IL-6 cytokine induced CD4+CD29+ subsets were found to provide effective helper function to B cells in IgG and IgM synthesis. CONCLUSION: The IL-6 production and IL-6 induced CD4+CD29+ T cell subset function in B cell antibody synthesis may be important in B cell hyperactivity and antibody synthesis in RA. Our studies suggest that CD4+CD29+ subsets bearing TcR gamma delta antigens are increased at inflammation site (SF) in RA and is implicated in immunopathology and autoantibody production of this inflammatory condition in humans.

Antigens, CD↗
PubMed1992

T-cell chronic lymphocytic leukemia. T-cell function and lymphokine secretion.

The leukemic T-cells of the six patients with T-cell chronic lymphocytic leukemia (T-CLL), four with CD4 and CD45R-positive (CD4+ CD45R*) T-CLL and two with CD8 and CD45R-positive (CD8+ CD45R+) T-CLL phenotype were studied for detailed immunologic phenotypic and functional characteristics. The levels of soluble interleukin-2 receptors were elevated significantly in the serum of all four patients with CD4+ CD45R+ T-CLL. Moreover, the CD4+ CD45R+ T-CLL patients' T-cells, after in vitro stimulation with phytohemagglutinin and concanavalin A, expressed elevated percentages of interleukin-2 receptors on cells and secreted high interleukin-2 activity. The B-cell growth factor (BCGF) activity from three patients with CD4+ CD45R+ T-CLL was enhanced, but B-cell differentiation factor (BCDF) activity of the all T-CLL patients was decreased. Reduced BCGF and BCDF activity of the leukemic T-cells was one possible mechanism of hypogammaglobulinemia detected in two patients with T-CLL. All T-CLL patients' leukemic T-cells had diminished immunoregulatory functional activity in allogeneic mixed lymphocyte reactions. These observations suggest that leukemic T-cells from T-CLL patients have many immunologic functional defects that may be important in their proliferative potential.

Aged↗
PubMed1992

Phenotype, activation and lymphokine secretion by gamma/delta T lymphocytes from schistosomiasis and carcinoma of the urinary bladder.

In humans the majority of the CD3+ T cells usually express an alpha/beta T cell receptor (TcR) and a minority express a gamma/delta TcR. The CD3+ TcR alpha/beta and CD3+ TcR gamma/delta cells from blood of the patients with schistosomiasis with carcinoma of the urinary bladder (SCB) were analyzed for phenotype, activation, secretion of interleukin 2 (IL 2). B cell growth factor (BCGF) and B cell differentiation factor (BCDF), as well as for autologous (AMLR) and allogeneic (MLR) mixed lymphocyte reaction. Patients with SCB had a highly increased percentage of CD3+ TcR gamma/delta and a decreased percentage of CD3+ TcR alpha/beta T cells in their circulation. These CD3+ TcR gamma/delta T cells expressed the CD25 (IL 2 receptor), CD38, CD71 (transferrin receptor) and HLA-DR activation antigens at a higher intensity after in vitro stimulation with recombinant IL 2, phytohemagglutinin and soluble egg antigen (from Schistosoma haematobium). The SCB patients' CD3+ TcR gamma/delta T cells were highly deficient in secretion of IL 2 but produced highly elevated levels of BCGF and BCDF. On the contrary, both BCGF and BCDF activities of the CD3+ TcR alpha/beta T cells were decreased. Moreover, CD3+ TcR gamma/delta T cells demonstrated highly deficient AMLR and MLR activity. These observations suggest a possible role of CD3+ TcR gamma/delta T cells in the immune response and the disease pathogenesis in human schistosomiasis infections.

Animals↗
PubMed1992

Gamma delta T cells and the immune response in visceral leishmaniasis.

Visceral leishmaniasis (VL) caused by Leishmania donovani, a protozoan parasite, is a disease of high morbidity associated with hepatosplenomegaly, hypergammaglobulinemia, fever and death. One of the immunological hallmarks of VL is a remarkable increase in serum immunoglobulin levels as a result of polyclonal B cell activation. This study demonstrated that T lymphocytes expressing the T cell receptors (TcR) gamma delta in association with CD3 molecules are increased in circulation of patients with VL. A large proportions of TcR gamma delta-bearing T cells had CD4+ CD8- phenotype, and expressed CD25, CD38, CD71 and HLA-DR activation antigens. Furthermore, we demonstrated wide functional differences in TcR gamma delta and TcR alpha beta T cells in their proliferative response, secretion of interleukin-2 (IL-2), B cell growth factor (BCGF) and B cell differentiation factor (BCDF). It was of interest that the TcR gamma delta T cells from patients with VL could be expanded by in vitro culture with human recombinant IL-2. Although these TcR gamma delta T cells secreted diminished levels of IL-2, they produced highly augmented levels of both BCGF and BCDF, suggesting that secretion of these lymphokines in these T cell subsets is regulated independently. The relative increases in the CD4+ CDw29+ TcR gamma delta T cell subsets and their secretion of highly elevated levels of BCGF and BCDF largely accounted for the humoral immune system abnormality and hypergammaglobulinemia found in this disease. These observations may help to explain that TcR gamma delta T cells might be functional in vivo and are involved in immunological mechanisms of pathogenesis in VL.

Antigens, CD↗
PubMed1992

T-cell receptor alpha/beta chain-CD3 protein complex defect in systemic lupus erythematosus: T-cell function.

We describe the first case of systemic lupus erythematosus (SLE) in which peripheral blood T cells were deficient in cell surface expression of T-cell receptor alpha/beta chain (TcR alpha beta) and the CD3 protein. Because of the uncommon phenotype and because of the notion that coexpression of TcR alpha beta and CD3 is essential for antigen-specific T-cell function, in vitro functional assays were performed, showing a highly decreased proliferative response to anti-CD3 antibody and other T-cell mitogens, deficient interleukin-2 (IL-2) secretion, and impaired function to respond in autologous and allogeneic mixed lymphocyte reactions. However, the helper-inducer function of T cells was unaffected by deficient expression of the TcR alpha beta/CD3 protein complex. The relative increase of CD4+ CDw29+ helper-inducer subsets in T cells accounted for elevated secretion of two terminal B-cell stimulating factors, B-cell growth factor (BCGF) and B-cell differentiation factor (BCDF). Hence, our results suggest that the regulation of secretion of lymphokines, IL-2, and BCGF and BCDF is independently controlled in T cells, and this case illustrates the pathologic sequelae of a unique defect in T cells characteristic of SLE.

Adult↗
PubMed1992

Soluble interleukin-2 receptor levels and immune activation in patients with schistosomiasis and carcinoma of the urinary bladder.

Soluble interleukin-2 receptor (sIL-2R) level in serum is a marker of immune regulation and lymphocyte activation. Highly elevated levels of sIL-2R in serum were observed in patients of schistosomiasis with carcinoma of the bladder (SCB) and carcinoma of the bladder without schistosomiasis (CB) compared with patients with carcinoma of the prostate with or without schistosomiasis and normal healthy controls. Patients with SCB, who had an elevated percentage of cells expressing CD38+ activation antigen and CD71+ transferrin receptors in circulation, also had elevated levels of sIL-2R in serum. There were few interleukin-2 receptor (CD25+) positive cells in circulation in some patients with SCB. Despite this, the sIL-2R levels were extremely elevated. Our data suggest that in SCB, CD38+ and CD71+ cells may be the source of secretion of sIL-2R in serum. This relationship was confirmed by phenotypic characterizations of mononuclear cells and sIL-2R levels in individual patients. Measurements of sIL-2R levels in serum may provide a sensitive method of immune activation in patients with SCB.

Antigens, CD↗
PubMed1991

Humoral immunodeficiency in T-cell chronic lymphocytic leukemia. An immunologic assessment.

The humoral antibody immunodeficiency in two patients with T-cell chronic lymphocytic leukemia (T-CLL) appeared to be the result of immunoregulatory abnormalities in the leukemic T-cell populations. Both patients had CD4+ CD45R+ "virgin" or suppressor-inducer T-CLL, but Patient 1 had hypogammaglobulinemia and Patient 2, immunoglobulin (Ig) M hypergammaglobulinemia. Although, CD25+ interleukin-2 (IL-2) receptors were present on leukemic T-cells of both patient, OKT9+ (CD71) transferrin receptors and OKT10 (CD38) activation antigens were found only on Patient 2's cells. Highly elevated amounts of IL-2 was secreted from phytohemagglutinin-stimulated and concanavalin A-stimulated T-cells in both patients. In Patient 1 with hypogammaglobulinemia, immune defects involve T-cells, first an intense suppressor activity on B-cell-induced IgM and IgG synthesis and, second, deficient production of B-cell growth factor (BCGF) and B-cell differentiation factor (BCDF). In Patient 2, highly elevated BCGF and IgM-specific BCDF was secreted by T-cells, a mechanism leading to IgM hypergammaglobulinemia in this patient. These studies stress the importance of BCGF and BCDF activity of leukemic T-cells in humoral antibody immunodeficiency disorders in T-CLL cases.

Aged↗
PubMed1991

T-cell abnormality and defective interleukin-2 production in patients with carcinoma of the urinary bladder with schistosomiasis.

Patients with schistosomiasis of the urinary bladder (SB) and schistosomiasis with carcinoma of the urinary bladder (SCB) had significantly increased percentage of IL-2R-, HLA-DR-, and transferrin receptor (T9)-bearing T cells in circulation. The percentage of these activated T cells decreased by in vitro culture with PHA but increased by Schistosoma haematobium soluble egg antigen. These patients with SB and SCB had a PHA-specific defect in IL-2 production. A functional defect with induction of IL-2R-positive suppressor monocytes appears to correlate with the defective PHA-induced IL-2 production by CD4+ T cells and monocytes. Disordered regulation of PHA-induced IL-2 production by the CD4+ T cells and monocytes may be the key feature in the highly depressed cell-mediated immune response in schistosomiasis. However, immune activation and significantly elevated IL-2 production in response to disease-specific S. haematobium soluble egg antigen may be related with the pathogenesis of SB and SCB. Thus, S. haematobium-specific CD4+ T cells are present in schistosomiasis, and their function is determined by adequate release of IL-2-and/or IL-2R-bearing CD11+ suppressor monocytes.

Adult↗
PubMed1991

Bacterial meningitis: T cell activation and immunoregulatory CD4+ T cell subset alteration.

Meningitis is the most important cause of acquired postnatal deafness and neurologic disorders in children. To determine if cell-mediated immunity is casually related to the pathogenesis of bacterial meningitis, T cell subsets were quantitated from blood of the 29 children with clinical and bacteriologic diagnosis of Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis bacterial meningitis. The CD4+ T cells increased and CD8+ T cells decreased in patients with meningitis as compared to patient control subjects (bacterial infections without meningitis) and normal healthy control subjects. An elevated percentage of CD25+ (interleukin-2 receptors) and HLA-DR+ (immune-response gene-associated antigen) T cells were detected from all patients with meningitis. All 29 patients with meningitis had highly elevated CD4+ CD45R+ (suppressor-inducer) cells and reciprocally depressed CD4+ CDw29+ (helper-inducer) cells compared with healthy age-matched normal and patient control subjects. These findings indicate characteristic immunologic T cell abnormalities from meningitis. The abnormal increase in the CD4+ CD45R+ suppressor-inducer or "virgin" cells and expression of activation antigens on T cells may be of help in future understanding of abnormal immune reactions from bacterial meningitis. However, deficiency of the CD4+ CDw29+ helper-inducer or "memory" cells may contribute to the impaired helper function for B cell-induced protective antibody synthesis to bacterial capsular polysaccharides found in this disease.

Antigens, CD↗
PubMed1991

Soluble interleukin 2 receptor levels in serum and its relationship to T cell abnormality and clinical manifestations of the disease in patients with systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is associated with alterations in immune regulation that results in T cell activation and release of the soluble interleukin 2 receptors (sIL-2R) in serum. SLE, a disease with varied clinical manifestations also has regulatory T cell subset abnormalities in blood. Levels of sIL-2R in serum of patients with active SLE were higher than in those with other common rheumatic diseases. Patients with active SLE and an increased percentage of CD4+ CDw29+ helper inducer (memory) and decreased percentage of CD4+ CD45R+ suppressor inducer (virgin) T cell subsets in blood demonstrated elevated levels of sIL-2R in serum. When compared with clinical manifestations of the disease, the sIL-2R levels in the sera of the patients with active SLE and thrombocytopenia were higher (mean 1710 units/ml) than those in active SLE with nephrotic syndrome (mean 1230 units/ml) or in active SLE with central nervous system disease (mean 1157 units/ml). However, patients with active SLE with humoral immunodeficiency (hypogammaglobulinemia) had highly elevated levels of sIL-2R in serum as compared to other patients with active SLE. The highly elevated levels of sIL-2R in serum may indicate that in vivo T cell activation plays an important role in this disease.

Adolescent↗
PubMed1991

Peripheral T-cell lymphomas. Immunophenotype, lymphokine production, and immunologic functional characteristics of the lymph-node malignant T cells.

Immunophenotype and functions of the malignant T cells to secrete various T-cell derived lymphokines and to respond in autologous mixed lymphocyte reaction (AMLR) and allogeneic mixed lymphocyte reaction (MLR) of the six patients with peripheral T-cell lymphomas (PTL) are presented. Three cases showed CD3/TcR alpha beta discordance (1 CD3+/TcR alpha beta-; 2 CD3-/TcR alpha beta+) and one showed absence of both these antigens (CD3-/TcR alpha beta-). In addition, we found that 50% of cases expressed CD25+, CD38+, and CD71+ activation antigens. The CD3/TcR alpha beta discordance and expressions of activation antigen noted in these cases were typical and similar to those reported from elsewhere. These malignant T cells from all cases whether CD25+ or CD25- (resting) expressed elevated interleukin-2 receptors (IL-2R) on stimulation with phytohemagglutinin (PHA) or human recombinant interleukin-2(rIL-2), and secreted elevated IL-2 by PHA, than do T cells from patients with tuberculosis (TB) or normal healthy controls. These malignant T cells also demonstrated elevated AMLR but deficient MLR B cells growth factor (BCGF) (except in one unusual case) secretion was increased, whereas B-cell differentiation factor (BCDF) secretion decreased. These results suggest that malignant T cells from lymph nodes of patients with PTL have uniform multiple immunologic defects in IL-2, BCGF, and BCDF lymphokine secretion and respond in AMLR and MLR, which do not correlate with immunophenotype or histologic types. These functions differentiate them from lymph-node T cells of patients with TB or blood T cells of normal healthy controls.

Aged↗
PubMed1990

Activated CD4-positive T-lymphocytes and impaired cell-mediated immunity in patients with carcinoma of the urinary bladder with schistosomiasis.

Patients with schistosomiasis of the urinary bladder (SB) associated with carcinoma of the bladder (SCB) or carcinoma of the prostate (SCP) have a variety of immunologic abnormalities, including the presence of HLA-DR+ and interleukin-2 receptor-positive (IL-2R+) T-lymphocytes in circulating blood. This study demonstrated that, the HLA-DR+ and IL-2R+ antigens are selectively expressed on majority of the CD4+ T-lymphocytes of patients with SCB, whereas, these antigens are expressed almost equally on both CD4+ and CD8+ T-lymphocytes of patients with SB and SCP. Expressions of HLA-DR+ and IL-2R+ antigens in CD4+ T-lymphocytes, and a depressed response of this T-cell subset to phytohemagglutinin and Concanavalin A stimulations seems to be the characteristic feature of these patients with SCB. In addition, the autologous mixed lymphocyte reaction (AMLR) and allogenic mixed lymphocyte reaction (MLR) was depressed in patients with SCB. However, patients with SCP demonstrated a normal MLR, even though the AMLR was highly depressed. The immunoregulatory role of the HLA-DR+, IL-2R+, CD4+ helper/inducer T-lymphocytes, and the AMLR and MLR abnormalities we have identified in patients with SCB may be important and could play a role in the pathobiology of these diseases in humans.

Adenocarcinoma↗
PubMed1990

Immune activation and T cell subset abnormalities in circulation of patients with recently diagnosed type I diabetes mellitus.

The peripheral blood lymphocytes from patients with insulin-dependent diabetes mellitus (IDDM) and healthy controls were analysed for the HLA-DR+, interleukin-2 receptor-positive (IL-2R+) activating antigens, and for CD45R+ and CDw29+ subsets from the purified CD4+ and CD8+ T cells populations. Patients with IDDM had an increased percentage of HLA-DR+ and IL-2R+ cells in both CD4+ and CD8+ T cells. However, the percentage of CD4+ CD45R+ suppressor/inducer T cells were decreased and CD4+ CDw29+ helper/inducer T cells increased in all patients with IDDM, compared with healthy controls. Thus, IDDM patients exhibit a deficiency in the CD4+ CD45R+ suppressor/inducer T cell subsets, which is probably related to the autoimmune phenomenon in this disease. In contrast, the percentage of CD8+ CDw29+ T cell subsets showed no major differences between patients with IDDM and controls. An alteration in the CD4+ CD45R+ and CD4+ CDw29+ T cell subsets appears to be a characteristic feature, and may relate to the impaired cell-mediated immunity in IDDM. These data provide new evidence for T cell dysregulation in IDDM.

Adolescent↗
PubMed1990

Immunoregulatory CD4+ CD45R+ suppressor/inducer T lymphocyte subsets and impaired cell-mediated immunity in patients with Down's syndrome.

The monoclonal antibodies 2H4 and 4B4 allow CD4+ and CD8+ T lymphocytes to be subdivided into CD45R+ and CDW29+ functional subpopulations. The CD4+ CD45R+ lymphocytes are designated as suppressor/inducer and CD4+ CDW29+ as helper/inducer subsets. Peripheral blood lymphocytes from 19 patients with Down's syndrome and 19 age- and sex-matched normal controls were analysed for the CD45R+ and CDW29+ subsets from the CD4+ and CD8+ T lymphocytes. The percentage of CD4+ CD45R+ cells (suppressor inducer) was markedly increased and of CD4+ CDW29+ cells (helper/inducer) decreased in all patients with Down's syndrome. In contract, the percentage of CD8+ CD45R+ and CD8+ CDW29+ subsets showed no major differences between patients with Down's syndrome and normal controls. Moreover, an alteration in the CD4+ and CD45R+ and CD4+ CDW29+ T cell subsets was accompanied by a markedly reduced proliferative response to phytohaemagglutinin and concanavalin A stimulation of the CD4+ T lymphocytes. Thus, a deficiency exists in patients with Down's syndrome in the CD4+ CDW29+ helper/inducer T cell subset which may contribute to their impaired cell-mediated immunity.

Antigens, Differentiation↗
PubMed1990

Increased circulating HLA-DR+ CD4+ T cells in systemic lupus erythematosus: alterations associated with prednisolone therapy.

Patients with active systemic lupus erythematosus (SLE) in the circulation have a selective increase of a subset of the CD4+ helper/inducer T cells bearing HLA-DR+, major histocompatibility complex class II antigens. We studied prednisolone-induced alterations of HLA-DR+, CD4+, and CD8+ T-cell subsets in three patients with active SLE. Prednisolone therapy was accompanied by a drastic reduction in circulating HLA-DR+, CD4+ T-cell subsets, serum anti-DNA titre, normalization of the serum immunoglobulin profile, and CD4+ T-cell responses to phytohaemagglutinin and concanavalin A. These changes in immune functions were associated with eventual improvement in the clinical condition of active SLE. A low percentage of HLA-DR+, CD8+ T-cell subsets was present in the circulation, which was not changed by prednisolone therapy. These results suggest that HLA-DR+, CD4+ T-cell subsets play a major role in the pathogenesis of active SLE, and that prednisolone-induced immunosuppression in this disease is mediated by changes in the HLA-DR+, CD4+ T-cell subsets in circulating blood.

Adult↗
PubMed1989

T cell malignancy in Richter's syndrome presenting as hyper IgM. Induction and characterization of a novel CD3+, CD4-, CD8+ T cell subset from phytohemagglutinin-stimulated patient's CD3+, CD4+, CD8+ leukemic T cells.

A patient is described, having Richter's syndrome and immunodeficiency with hyper IgM, who developed suppressor T cell lymphoma (CD3+, CD4-, CD8+) following untreated helper-suppressor T cell chronic lymphocytic leukemia (CD3+, CD4+, CD8+). The neoplastic T cells in both malignancies expressed interleukin (IL) 2 receptors but were deficient in typical CD2+ and CD5+ pan T antigens. Additionally, a large percentage of malignant lymph node T cells expressed HLA-DR+ activation antigens. In vitro immunoglobulin-production experiments demonstrated that the patient's leukemic blood T cells had an excess helper function for IgM synthesis but a suppressor function for IgG and IgA synthesis by normal B and T cells. The leukemic blood T cells demonstrated a poor response to phytohemagglutinin (PHA). A defect in IL 2 receptor expression was evident in PHA-stimulated leukemic blood T cells. Of interest was the observation that PHA stimulated the induction of a novel CD3+, CD4-, CD8+ T cell subset from patient's CD3+, CD4+, CD8+ leukemic blood T cells. These PHA-induced CD3+, CD4-, CD8+ T cell subsets produced an elevated proliferative response to PHA and concanavalin A, had a helper cell function for IgM synthesis and produced highly elevated amounts of IL 2.

Aged↗