Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Depression of cell-mediated immunity is well established in most malignancies and especially in head and neck cancers, and much information is available concerning the defect in helper T lymphocyte function. We now report on impairment of the monocyte-macrophage system. Compared with normal controls we found that patients displayed, on one hand, an increased number of peripheral blood monocytes and, on the other hand, a smaller percentage of HLA-DR+ monocytes. Such peripheral blood monocytes normally failed to secrete factors, including interleukin 1 (IL-1). In addition, we observed that the in vivo induced blastogenesis of peripheral blood lymphocytes from patients, which is spontaneously depressed, is partly restored by medium containing IL-1. We cannot exclude, however, that the observed monocyte dysfunction involves other cytokines. Whether such an immune deficiency is due to secondary malnutrition or to the malignancy (or both) remains unclear.
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PMID:Impairment of monocyte functions in advanced head and neck cancer. 326 77

The production of procoagulant activity by circulating monocytes and its regulation by a cytokine secreted by mitogen-stimulated peripheral blood mononuclear cells was investigated in recipients of HLA-identical sibling bone marrow transplants. Blood monocyte numbers reached the normal range within 3 weeks of transplant. After stimulation with lipopolysaccharide, macrophage procoagulant activity was found to be within the normal range in all patients at all times post transplant. It did not appear to correlate with the presence or absence of graft-versus-host disease. Surprisingly, and in marked contrast to our previously documented severe depression of interleukin 2 production by transplant recipients' peripheral blood mononuclear cells, the mitogen-induced production of the cytokine that induces procoagulant activity production (macrophage procoagulant inducing factor, MPIF) was also normal in the majority of patients when assayed using the responsive myelomonocytic cell line RC-2A. These findings suggest firstly that monocyte differentiation and function normalize rapidly post transplant; and secondly, when taken together with previous studies, that the ability of peripheral blood mononuclear cells to synthesize cytokines post transplant varies greatly according to the specific cytokine involved.
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PMID:Cytokine activity after human bone marrow transplantation. II. Production of macrophage procoagulant activity and the cytokine regulating its production, macrophage procoagulant inducing factor. 329 28

Natural killer (NK) activity was assessed in a prospective fashion in 15 renal transplant recipients receiving single HLA-haplotype matched allografts and maintained on cyclosporine (CYA) immunosuppression. There was marked variability in NK activity pretransplantation in this population; however, a strong correlation (r = 0.92, p less than 0.01) was found between determinations in an individual patient upon repeated testing. No significant depression of NK activity occurred within the first 12 weeks following transplantation. Whole blood CYA levels did not correlate with NK activity. Although NK activity prior to transplantation did not predict clinical outcome of the allograft, a marked rise in NK activity was observed in patients undergoing rejection compared with those not rejecting (p less than 0.01). A large increment in activity was seen in eight of 11 rejection episodes; a similar increase was rarely seen in the absence of rejection. These results indicate that NK activity is stimulated during allograft rejection in CYA treated renal transplant recipients. It remains to be determined whether this rise in NK function represents a manifestation of alloreactivity accompanying the rejection process or whether NK cells directly contribute to allograft destruction.
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PMID:Increase in natural killer activity in cyclosporine-treated renal allograft recipients during rejection. 330 57

Normal human peritoneal macrophages show a restricted capacity to differentiate into inflammatory macrophages in vivo. We now report that these cells are unable to cap and internalize HLA-DR, as compared to endometriosis, and other macrophages. Immunoelectron microscopy indicated that lack of modulation was not due to the presence of preclustered antigenic sites. Northern blot analysis demonstrated transcripts for HLA.DR, c-fms, and c-fos, indicating that the surface defects were not likely to be associated with a general depression of transcriptional activity. There was no correlation between the mobility of class II molecules and the ability to present antigen as determined by autologous lymphocyte responses to tetanus toxoid. The inability of normal peritoneal macrophages to modulate class II antigens may represent a normal and more general environmental alteration required to permit peritoneal cells a scavenging function without developing the deleterious effects leading to a peritoneal inflammatory response.
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PMID:Normal human peritoneal macrophages are unable to cap and internalize class II antigens. 340 27

An examination was made of blastogenic response to phytohaemagglutinin (PHA) in HLA-B8 and/or DR3 positive subjects and B8/DR3 negative individuals. Both B8 and DR3 antigens were associated with a depression of the response at all three doses of PHA used. The possession of both these antigens did not lead to a further depression of the response.
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PMID:Impaired lymphocyte responsiveness to phytohaemagglutinin associated with the possession of HLA-B8/DR3. 349 78

The relationship of some clinical, personality and biological variables to the outcome of lithium prophylaxis was investigated in two patient samples fulfilling, respectively, the DSM III definitions of "major depression, recurrent" and "bipolar disorder". In major depressives, the presence of psychomotor retardation and melancholia during the index episode was associated with a favorable response to treatment, whereas the presence of mood-incongruent psychotic features during the same episode, a high score on the "anxiety" and "phobic" subscales of the Middlesex Hospital Questionnaire and a high score on the "neuroticism" subscale of the Eysenck Personality Questionnaire were related to a poor response. These findings are discussed in the light of the heterogeneity of DSM III major depression and of the reported common occurrence of an "anxiety-phobic" personality profile in unipolar depressives. In bipolar patients, a family history of bipolar affective illness and a high lithium ratio were associated with a good response to treatment, and the presence of the HLA-A3 antigen with an unfavorable response. These findings seem to support a role of pharmacogenetic factors in conditioning response to lithium prophylaxis.
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PMID:Factors associated with response to lithium prophylaxis in DSM III major depression and bipolar disorder. 393 Nov 8

We cultured immunosuppressor T cells from gastric cancer patients using T-cell growth factor (TCGF) prepared from human tonsil or spleen. Peripheral blood lymphocytes cultured for 3-4 weeks with TCGF strongly inhibited the lymphocyte-proliferative response to alloantigen or PHA. Quantitative fluorescence measurement for immunological analysis of phenotypic characterization of the cells was made on a FACS-IV, using monoclonal antibodies (anti Leu-I, anti Leu-2a, anti Leu-3a, anti Leu-4, anti Leu-5, anti Leu-7, anti HLA-DR) and goat anti-human immunoglobulin. Immunosuppressor T cells grown in the presence of TCGF showed phenotype Leu-1+, 2a+, 3a-, 4+, 5+, 7-, HLA-DR+, human Ig-. Culture of immunosuppressor T cells activated by tumor cell antigen in vitro was successful only when the cells derived from patients with disseminated, nonresectable type of gastric carcinoma. Our findings suggest that TCGF-dependent immunosuppressor T cells are the result of a large tumor burden; this may explain the depression of in vitro or in vivo cell-mediated immune responses frequently found in such cancer patients.
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PMID:[Culture of TCGF-dependent immunosuppressor T cells in gastric cancer patients and phenotypic characterization of the cell surface, using monoclonal antibodies and a fluorescence-activated cell sorter (FACS)]. 623 8

Reactive arthritis is arthritis in which, although the nature of the responsible infection is known or suspected upon serological grounds, attempts at recovering the pathogen from the synovial fluid have failed. One of the main pathogenetic problems is the multiplicity of etiologic agents. Some are exogenous and may be related to the articular tropism of certain microorganisms, to immunologic depression due to an antecedent or coincident infection, and to successive reinfections by the same pathogen or by others which may promote an exacerbation of the disease. Others are endogenous and attention should be given to the local or systemic presence of an antigen as well as, in some instances, to the persistence of residual forms of infecting agents, which are more readily demonstrated with current bacteriological and serological methods. Although reactive arthritis is to be distinguished from septic arthritis, it can no longer be clearly differentiated from the classical post-infectious rheumatism. Once it has been produced, the antigenic stimulation is responsible for an immunologic response which tends to check systemic extension but may also produce tissue damage in the host. Some patients have circulating immune complexes which may bind to the joint, thereby damaging it. In other patients, particularly those who are HLA B27 positive, host-pathogen cross-reactions are demonstrated. Actually, the most frequent pathogenetic sequence seems to be a combination of two or more of these mechanisms, as there are reasons to believe that presence of the pathogen in situ is not required for the persistence of the inflammatory process. Reactive arthritis was first reported in adults following either sexually transmitted urethritis due to chlamydiae, mycoplasma or gonococci, or hepatitis B or an intestinal infection due to Yersinia, Campylobacter, Shigella, Klebsiella or Salmonella. Later, it was described in pediatric patients, particularly in Scandinavia where, for genetic reasons, the HLA B27 group is prevailing. Reactive arthritis seems less frequent in caucasian ethnic groups and above all in Latin Americans among whom HLA B27 carriers are more uncommon; however, it must be pointed out that they have not been as extensively studied and that other etiologic factors may still remain to be discovered. The course and etiology of the different forms of arthritis share certain characteristics which have been determined through a better knowledge of these conditions: onset occurs one or several weeks after a respiratory, urinary or, most often in children, digestive infection. This episode is unremarkable or latent and often overlooked.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Reactive arthritis in children]. 632 Apr 36

Peripheral blood derived macrophages from lepromatous leprosy patients were unable to interact with lymphocytes in the presence of M. leprae. This lack of interaction is probably not associated with membrane HLA-Dr antigens since trypsin and colchicine restored M. leprae induced depression in the latter but were unable to bring about a positive interaction. Two possible defects exist therefore in the lepromatous macrophage. These are an innate inability to process and present M. leprae antigens to lymphocytes and an induced inability to express some membrane receptors, an event detrimental to the normal functioning of a macrophage.
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PMID:Antigen specific macrophage-lymphocyte interaction in lepromatous leprosy. 637 10

A long-term epidemiological genetic study was conducted in which all new patients were evaluated prospectively at the Foundation for Depression and Manic Depression and two Lithium/Affective Disorders clinics at the Columbia-Presbyterian Medical Center between the years of 1972 and 1978. All patients met Feighner, RDC and DSM III criteria for Major Depressive Disorder after initial clinical screening interviews and were further subtyped using the Fieve-Dunner 7-point criteria. All 604 probands and 90% of 2711 first-degree relatives were interviewed blindly by diagnosticians trained in the use of the SADS structured interview. Cumulative morbid risk in parents, siblings and children of 490 bipolar probands was 15.6 +/- 3% and 14.0 +/- 1.7% in the first-degree relatives of 114 unipolar probands. A number of biological and genetic marker studies were simultaneously performed on samples of the overall population. The enzymes catechol O-methyltransferase and dopamine beta-hydroxylase, and the dexamethasone suppression test (SDT) did not show any biological marker value for outpatients even though both enzymes were determined to have hereditability. The HLA system, monoamine oxidase and acetylcholinesterase segregated differently from normal controls in samples of the patient population. The positive association findings with monoamine oxidase and the HLA system conflicted with the positive findings of other investigators, leaving doubtful their biological marker value. Red cell acetylcholinesterase was found to be significantly lower in affective disorder patients than in controls. This positive association finding was recently replicated by Mathews et al. (1982) but needs further confirmation. Using 28 blood group markers, a prior association study between the trait defining susceptibility to affective disorder and the genetic marker was positive for haptoglobin GC, and properdinfactor B, confirming earlier findings. Using the sib-pair method on the remaining 25 blood groups revealed that none other than peptidase A showed significant linkage with affective disorder since one significant finding is expected by chance. We conclude from the overall morbid risk data and segregation analyses that bipolar manic-depressive illness is a spectrum disease inherited through a multifactorial mode of genetic transmission (which is not synonymous with polygenetic inheritance) with possible genetic heterogeneity and find no evidence for X-linkage. Additional studies with acetylcholinesterase, haptoglobin, GC, and properdin-factor B are needed to confirm their positive biological/genetic marker value suggested by our long-term epidemiological study.
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PMID:Search for biological/genetic markers in a long-term epidemiological and morbid risk study of affective disorders. 651 12


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