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)

Prostaglandins are said to influence T and B cell function by inhibiting the generation of interleukin 2 (IL 2) and the formation of suppressor lymphocytes. After bone marrow transplantation, patients usually have a profound immunodeficiency that persists in recipients with chronic graft-v-host disease (GVHD) and generally resolves in long-term survivors without GVHD. In vitro tests of lymphocyte function such as allogeneic mixed lymphocyte culture (MLC) and cell-mediated lympholysis (CML) have been shown to be impaired in many patients. We postulated that prostaglandin E2 (PGE2) plays a role in the impaired in vitro tests. To test this hypothesis, we studied in vitro tests in the presence of PGE2 antagonists, indomethacin, and anti-PGE2 antiserum with cells from 22 short-term patients (less than 100 days postgrafting) and 32 long-term survivors with or without GVHD. Results show that blockade of PGE2 release by indomethacin and anti-PGE2 significantly (P less than .01) enhanced the MLC (+67%) and the CML responses (+10.5%) of cells from long-term survivors with chronic GVHD but not from those of long-term, stable recipients. No enhancement of MLC and CML activity was observed with cells from donors of long-term recipients. In patients shortly after marrow grafting, enhancement in the MLC was not significant. However, CML activity in this patient group was significantly increased (+12.5% in recipients with no GVHD, 8.5% in those with acute GVHD, P less than .01). Indomethacin also suppressed the activity of nonspecific suppressor cells in patients with chronic GVHD. When cells from patients with chronic GVHD were treated with recombinant IL 2 and IL 2 combined with indomethacin, it was possible to get an additional augmentation of lymphocyte proliferation after the addition of indomethacin to IL 2-treated cultures. Thus it is very likely that PGE2 inhibits T lymphocyte proliferation, not exclusively by inhibition of IL2 production or activity. We conclude that PGE2, among other factors, may play a role in the pathogenesis of the immunodeficiency after transplantation. PGE2 does not act primarily by interfering with IL2 but presumably by inducing a suppressorlike activity.
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PMID:Inhibition of prostaglandin E2 restores defective lymphocyte proliferation and cell-mediated lympholysis in recipients after allogeneic marrow grafting. 294 Oct 83

The authors recently measured the Interleukin-1 (IL-1) and Prostaglandin E (PGE) activity of the monocyte-macrophage system (M phi) in vitro. The results indicated that immunodeficiency in cancer patients is closely associated with reduced IL-1 activity and increased PGE activity of M phi. Immunosuppressive factors in the serum of cancer patients seem to play some role in the mechanism of such change. Therefore, when potentiating M phi in nonspecific immunotherapy, it seems important to suppress secretion of PGE (a suppressor factor of M phi origin which is secreted simultaneously) to make this therapy more effective in advanced cancer cases. Based on these results, an animal experiment was carried out in which tumor-bearing mice were treated with OK-432 and Indomethacin (Ind.) (a PG inhibitor). The results of this experiment suggested that this combination therapy reinforces the M phi-mediated immunopotentiation, resulting in a stronger antitumor effect of OK-432. When we used this combination therapy in advanced cancer cases, the changes observed in immunological parameters also indicated an immunopotentiating effect, i.e., an antitumor effect. These results indicate that the optimum application of BRM therapy should be decided on the basis of an understanding of the immunological factors in the patient.
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PMID:Immunomodulating capacity of the monocyte-macrophage system in patients with uterine cervical cancer. 326 Feb 61

Hypoimmunity after major trauma and thermal injury appears to predispose to septicemia. An increase of immune suppressive T cells and the inhibitory monocytes product PGE2 has been demonstrated postburn and are suggested as contributing to postburn hypoimmunity. TP5, the biologically active part of thymopoientin, has an immunomodulating effect on T cells. Indomethacin, an irreversible blocker of the prostaglandin synthesis has been suggested to reduce the inhibitory monocytes-mediated immunosuppression. In this study strains 2 and 13 guinea pigs received 20-30% TBSA scald burn and were subsequently injected with either TP5 or indomethacin or a combination of both on the 3 following days postburn. The ability of splenocytes to produce a secondary immune response to SRBC was measured in the in vitro AFC assay. The animals who had received TP5 and indomethacin showed significant improvement in their ability to mount an immune response in the AFC assay.
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PMID:The immunomodulating effect of TP5 and indomethacin in burn-induced hypoimmunity. 623 2

We report on an uncommon laryngeal non-Langerhans cell histiocytosis. An 11-year-old boy presented with a 6 months history of progressive breath inhibition. Magnetic resonance imaging showed diffuse laryngeal and local lymph node swelling. Histology first resembled sarcoidosis, however, corticosteroids were ineffective. Lymphoma, infection, immunodeficiency, and autoimmune disease were excluded. Six months later, biopsies were repeated, now showing numerous ectatic lymph vessels with clusters of histiocytes bearing stellate extensions and emperipolesis. S100 protein and CD1a were negative. Indomethacin treatment led to a gradual improvement. In conclusion, we observed a nonmalignant non-Langerhans cell endolymphatic reticulohistiocytosis, not fitting into any of the described categories.
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PMID:Endolymphatic non-langerhans cell histiocytosis of the larynx: report of an uncommon disease manifestation. 2046 9