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)

Intravenous injection of LPS or allogeneic lymphocytes resulted in impaired maturation of B cells within the bursa of chick embryos. A gradual decline in the sensitivity of embryos towards both agents was reflected by a decrease in the number and size of bursal follicles following injection between 10 and 15 days of embryonation. The hypoplasia of these follicles in embryos injected with lymphocytes on the 10th day was a more sensitive measure of graft-versus-host reaction than splenomegaly. The relevance of results with this model to the aetiology of immunodeficiency diseases has been briefly discussed.
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PMID:Immunodeficiency in the chicken. III. Hypoplasia of bursal follicles following intravenous injection of embryos with lipopolysaccharide or allogeneic lymphocytes. 23 84

LP-BM5 murine leukemia virus (MuLV) induces an immunodeficiency syndrome (MAIDS) in C57BL/6 mice which resembles immunological abnormalities observed in early stages of human AIDS. In our study, MAIDS virus-infected mice were exposed to low doses of ultraviolet radiation (UVR) before and after virus inoculation and compared with MAIDS-infected but not UVR-exposed mice. In all tested parameters (blood IgM levels; mitogenic responses to PHA, ConA, LPS and anti-mu; MLR; antigenic response to SRBC; enlargement and histopathologic changes of the spleen) we observed the same trend: changes due to MAIDS infection were more pronounced in the UVR-exposed group than in the unexposed group. Statistically significant differences between these two groups were seen for mitogenic responses at two different time points after virus inoculation. These results demonstrate that in vivo UVR exposure enhances the immunosuppressive effects of a retroviral infection. UVR exposure may affect the progression of AIDS in a similar manner.
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PMID:In vivo exposure to ultraviolet radiation enhances pathogenic effects of murine leukemia virus, LP-BM5, in murine acquired immunodeficiency syndrome. 133 87

To test the hypothesis that the lung represents a source of interleukin (IL)-6 in human immunodeficiency virus type 1 (HIV-1)-positive subjects, alveolar macrophages (AM) obtained from the bronchoalveolar lavage (BAL) fluid of 10 HIV-1-positive patients were investigated for the expression of IL-6 mRNA and the ability to release IL-6. The presence of IL-6 in BAL fluid was also investigated. It has been demonstrated that freshly recovered AM from HIV-1-positive patients show a strong IL-6 mRNA signal. The message for IL-6 increases following culture with LPS. Supernatants obtained from AM cultured in medium alone contain high amounts of IL-6; the values are three to four times higher following culture with LPS. IL-6 has also been detected in the BAL fluid from 5 of 8 HIV-1-positive patients. Results of immunoblotting analysis were consistent with those given above. These findings suggest that the lung represents a source of IL-6 production in HIV-1-infected subjects with lung disorders.
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PMID:Spontaneous production of interleukin-6 by alveolar macrophages from human immunodeficiency virus type 1-infected patients. 152 8

We studied the release of tumor necrosis factor-alpha (TNF alpha), a vital immunoregulatory cytokine, by alveolar macrophages (M phi s) infected with simian immunodeficiency virus (SIV) in vitro or collected from SIV-infected macaques. For in vitro studies, M phi s were harvested by bronchoalveolar lavage from 5 normal animals and infected in flasks with SIV (10(4)TCID50/2.5 x 10(6) M phi s). After 7 to 10 days, cytopathic effect was prominent and 68 +/- 2% of M phi s were immunoreactive for p27 core protein. Uninfected (control) and SIV-infected M phi s were then cultured for 24 hours in 96-well plates (10(5) M phi s/well) while challenged with lipopolysaccharide (LPS; 100 micrograms/ml). TNF alpha was assayed in culture supernatants by an enzyme-linked immunosorbent assay (detection limit, 50 pg/ml) and results were expressed as pg TNF alpha/ml/10(3) M phi s (mean +/- SEM). TNF alpha was not detected in unstimulated wells. TNF alpha release by control and SIV-infected M phi s was similar (6.6 +/- 0.7 and 7.9 +/- 1.1 pg/ml/10(3) M phi s, respectively). We also studied TNF alpha release by alveolar M phi s from 8 animals infected with SIV (3 asymptomatic, 5 with acquired immune deficiency syndrome virus (AIDS]. One animal with AIDS had p27+ M phi s. Alveolar M phi s from asymptomatic animals released significantly more TNF alpha (10.3 +/- 1.1 pg/ml/10(3) M phi s) than did animals with AIDS or uninfected macaques (5.2 +/- 0.8 and 7.0 +/- 0.6 pg/ml/10(3) M phi s, respectively) (p less than 0.01). However, M phi s from monkeys with AIDS failed to respond to LPS after 7 to 10 days in culture. In summary, in vitro infection with SIV does not cause constitutive TNF alpha release or alter the response of cultured M phi s to LPS. When kept in culture, M phi s collected from asymptomatic, SIV-infected animals retain their response to LPS, whereas M phi s from animals with AIDS lose the capacity to produce TNF alpha. Furthermore, M phi s cytokine production is exaggerated before overt clinical disease, but not as a direct result of infection with SIV.
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PMID:Effect of simian immunodeficiency virus infection on tumor necrosis factor-alpha production by alveolar macrophages. 189 Aug 5

Studies with FLV infected mice, a model for retrovirus induced acquired immunodeficiency, showed that intact lipopolysaccharide rich extract from Serratia marcescens as well as the nontoxic polysaccharide derivative free of lipid A were equally adjuvantic in enhancing antibody formation to sheep erythrocytes, both in vivo and in vitro. The PS-rich endotoxin derivative had little or no toxic activity in leukemic animals as occurred with intact endotoxin. The adjuvanticity of both the nontoxic polysaccharide derivative as well as the intact endotoxin in enhancing antibody formation in FLV infected mice was evident also in vitro when spleen cells from infected animals were immunized with sheep erythrocytes simultaneously with the polysaccharide in comparison with the LPS. Supernatants from normal spleen cells treated in vitro either with the polysaccharide or the intact endotoxin showed immunoenhancing helper activity for both normal and FLV infected spleen cells and this enhancing activity was due to IL-1 induced by either bacterial product. Thus the immunoenhancing soluble mediator, i.e., IL-1, is induced equally by PS or LPS and has immunorestorative activity for FLV infected animals. The potential value of the nontoxic PS as an immunoadjuvant in retrovirus immunosuppressed lymphoid cells is evident. The results of these studies suggest that further investigations concerning the nature and mechanism involved in such adjuvancticity is warranted.
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PMID:Immunoadjuvanticity of endotoxins and nontoxic derivatives for normal and leukemic immunocytes. 218 63

Expression of tumor necrosis factor (TNF alpha), tissue factor (TF), and interleukin 1-beta (IL-1 beta) mRNA was evaluated in monocytes isolated from patients infected with human immunodeficiency virus (HIV). There was a significant depression (66%) of the induced level of TF mRNA expression in response to lipopolysaccharide. Conversely, the response of TNF alpha and IL-1 beta, following LPS induction, was "normal." TF mRNA reduction was also observed to a lesser degree in AIDS-related complex patients (20%) but not in asymptomatic seropositives. TF is necessary for initiation of the coagulation protease cascade, leading to thrombin production and fibrin deposition, which play a role in inflammatory responses. Its selective reduction may be a factor in the diminished resistance to secondary infections observed in AIDS. Further, since the TF defect increases as patients progress toward AIDS, it may serve as a marker for disease progression.
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PMID:A selective defect in tissue factor mRNA expression in monocytes from AIDS patients. 229 2

CBA/N mice, which express the X-linked immunodeficiency gene xid, are susceptible to Salmonella typhimurium. The basis for this susceptibility is currently unknown. However, previous studies (10) from this laboratory have provided evidence that susceptibility may be due to a defective anti-S. typhimurium antibody response. In that report we hypothesized that the defective antibody response may be a reflection of an altered S. typhimurium-specific B cell repertoire. In the studies described here, we have investigated this hypothesis using a modification of the in vitro splenic focus system. The frequency and characteristics of salmonella-specific B cells in normal, innately resistant, CBA/Ca mice have been compared with those of salmonella-susceptible, anti-S. typhimurium antibody-defective CBA/N mice. The results show that CBA/N mice express no primary or secondary S. typhimurium-specific B cell precursors after stimulation with an acetone-killed and dried (AKD) preparation of S. typhimurium strain TML. However, after three immunizations, the CBA/N tertiary frequency of 15.4 per 10(6) splenic B cells was similar to the primary precursor frequency in immunologically normal CBA/Ca mice, but 23-fold lower than the tertiary precursor frequency in CBA/Ca control mice. Moreover, CBA/N mice had an altered isotype distribution pattern after stimulation with AKD-TML. Greater than 70% of the tertiary CBA/N TML-specific B cells secreted IgG2, in contrast to either nonimmune or primed control mice. In addition, 80% of the CBA/N TML-specific B cells secreted only a single isotype, whereas the majority of B cells from primed normal mice secreted multiple isotypes. Fine specificity analysis of the TML-specific B cells indicated that the array of antigenic determinants to which CBA/N B cells could respond was restricted. Although the majority of primed CBA/Ca and primed CBA/N B cells were specific for LPS, the fine specificity pattern exhibited by CBA/N B cells was similar to that observed in unprimed normal mice, i.e., the vast majority were specific for the O antigen region of the LPS molecule. In contrast, a major portion of the LPS-specific B cells in primed CBA/Ca mice were directed against the KDO/lipid A region of the LPS molecule. Therefore, it appears that CBA/N mice lack or are unable to stimulate the B cell subset that predominates in primed, normal mice. Taken together, these studies indicate that the basis for susceptibility of CBA/N mice to S. typhimurium is multifactorial and suggests that the inability of some animals to respond to some infectious agents may be related to holes in their B cell repertoire.
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PMID:Antibody-defective, genetically susceptible CBA/N mice have an altered Salmonella typhimurium-specific B cell repertoire. 243 51

Alloreactive mixed lymphocyte reaction (MLR), mitogen-induced response (MR), and suppressor cells against these responses in murine bone marrow chimeras were examined, to clarify the mechanisms of immunological tolerance and immunodeficiency after bone marrow transplantation (BMT). Between 35 and 70 days after BMT, there was no response of spleen cells from allogeneic chimeras against host (C3H/He) and donor (BALB/c) cells, although responses against third party (C57BL/6) cells were detected, thus indicating that these allogeneic chimeras were immunologically tolerant. The activity of suppressor cells against alloreactive responses was increased 35 to 55 days after BMT, so that these suppressor cells appeared to be related to immunological tolerance. Some of the suppressor cells against alloreactive responses were Thy1+. Among them some were Lyt1+ or Lyt2+, and others were Lyt1+2+. Plastic dish non-adherent cells had slightly weaker suppressor activity than adherent cells. Proliferative responses to Con A, PHA, and PWM were decreased 13 to 15 days after BMT, and gradually increased. The responses to LPS differed from those to the former three mitogens, showing an enhanced response 21 to 25 days after BMT. The increased response to LPS did not appear to be simply due to the increased number of non-T cells in the spleen of allogeneic chimeras. The alloantigen specific suppressor cells may play an important role in the induction and maintenance of immunological tolerance, while the alloantigen nonspecific suppressor cells and suppressor cells against MRs may be related to immunodeficiency after BMT.
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PMID:[Alloreactivity and mitogen-induced responses in allogeneic murine bone marrow chimeras]. 253 28

Atopic dermatitis (AD) represents an inflammatory skin disorder which is characterized by many signs of immunodeficiency. Particularly, decreased lymphoproliferative responses upon stimulation with mitogens as well as bacterial antigens were reported repeatedly. Since there is increasing evidence for a network of immuno-modulating cytokines playing a crucial role in the regulation of immunity and inflammation, in the present study we investigated whether an altered production of these mediators is one of the pathomechanisms responsible for the altered immune response in AD. For this purpose the 24-h supernatants of LPS- and PHA-stimulated or unstimulated mononuclear cells (MNC) from patients with AD of a moderate to severe disease activity and from nonatopic healthy controls were tested for Interleukin-1 (IL-1) and Interleukin-2 (IL-2) activity. Whereas supernatants of unstimulated MNC of AD patients and controls did not contain significantly different levels of these cytokines, LPS-stimulated MNC of AD patients released significantly less IL-1 in the supernatants. Similarly, the production of IL-2 by PHA-stimulated MNC of AD patients was significantly decreased in comparison to the controls. Moreover, there was a strong correlation between IL-1 and IL-2 levels. These findings indicate that diminished lymphoproliferative responses in AD may partly be caused by a decreased capacity of MNC to release immuno-modulating cytokines, even upon appropriate stimulation.
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PMID:Altered production of immuno-modulating cytokines in patients with atopic dermatitis. 280 Sep 14

Suppressor cells against several mitogen-induced responses were detected in the spleen of murine bone marrow chimeras, regardless of intravenous (i.v.) or intrasplenic (i.s.) bone marrow transplantation (BMT). According to the time-course of the suppressor activity against Con A, PHA, and PWM, they were readily detected at 11-21 days after BMT and thereafter, either gradually decreased or remained at a plateau level. In contrast, the suppressor activity against the LPS-stimulated response increased at 39-52 days as compared to 24-34 days after BMT. Characterization studies of suppressor cells early (11-21 days) after BMT revealed that those in the i.v. and i.s. chimeras were composed of host-derived plastic dish adherent and/or anti-Thy 1.2 antibody-insensitive spleen cells in general. On the contrary, those in the i.v. and i.s. chimeras that possessed severer GVHD were mainly composed of host-derived plastic dish non-adherent spleen cells. Since the suppressor activity was higher in chimeras with severe graft-versus-host disease (GVHD) than in conventional chimeras, suppressor cells against the mitogen-induced responses may be related to the immunodeficiency associated with GVHD. Particularly, plastic dish non-adherent suppressor cells may closely relate to GVHD-associated immunodeficiency as compared with plastic dish adherent suppressor cells.
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PMID:Non-specific suppressor cells in murine bone marrow chimeras: their possible role in GVHD-associated immunodeficiency. 296 5


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