| pubmed-article:7525297 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7525297 | lifeskim:mentions | umls-concept:C0026918 | lld:lifeskim |
| pubmed-article:7525297 | lifeskim:mentions | umls-concept:C0567416 | lld:lifeskim |
| pubmed-article:7525297 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:7525297 | lifeskim:mentions | umls-concept:C0007582 | lld:lifeskim |
| pubmed-article:7525297 | lifeskim:mentions | umls-concept:C1318468 | lld:lifeskim |
| pubmed-article:7525297 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:7525297 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
| pubmed-article:7525297 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
| pubmed-article:7525297 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:7525297 | pubmed:dateCreated | 1994-12-21 | lld:pubmed |
| pubmed-article:7525297 | pubmed:abstractText | The most important immunopathological consequence of experimental mycobacterial infection is the suppression of T cell-mediated immune response to both mitogens and mycobacterial antigens. We registered that there was decreased concanavalin A-induced spleen cell proliferation in infected susceptible BALB/c mice as compared to normal mice. In resistant (C3H/HeJ) mice, infection with the bacteria did not induce any suppression in the mitogen-induced lymphoproliferation. Likewise, delayed-type hypersensitivity (DTH) responses, to keyhole limpet hemocyanin and mycobacterial crude soluble antigen were suppressed in infected BALB/c mice but not in C3H/HeJ mice. This depressed T helper cell function may either be due to defective T cell-receptor occupancy by antigen-Ia complex or altered co-stimulatory signals provided by antigen-presenting cells. In the present study, we have investigated the status of certain co-stimulatory molecules on the infected macrophages from both susceptible and resistant mice. Our results demonstrate that upon mycobacterial infection, the macrophages are rendered incapable of delivering the co-stimulatory signals to T helper cells, possibly due to the involvement of prostaglandin, as inhibition of its biosynthesis by indomethacin reversed the defect. Furthermore, the selective regulation was bacteria-induced as killing of the bacteria by rifampicin abrogated the derangements in the expression of co-stimulatory molecules on the Mycobacterium-infected macrophages. Our observations revealed that upon infection with Mycobacterium tuberculosis, B7 was down-regulated while ICAM-1 was increased only in BALB/c but not in C3H/HeJ mice. Expression of VCAM-1 did not change during the infection in either strain of mice. We found that these changes in ICAM-1 and B7 expression on the surface of infected macrophages resulted in inhibition of DTH-mediating functions of T helper cells from BALB/c mice. The results obtained in this study describe not only a novel immune evasion strategy adopted by Mycobacterium, but also open up the possibility of immunotherapy of mycobacterial infection by selective manipulation of co-stimulatory molecules. | lld:pubmed |
| pubmed-article:7525297 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7525297 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7525297 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7525297 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7525297 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:7525297 | pubmed:issn | 0014-2980 | lld:pubmed |
| pubmed-article:7525297 | pubmed:author | pubmed-author:GangulyN KNK | lld:pubmed |
| pubmed-article:7525297 | pubmed:author | pubmed-author:MishraG CGC | lld:pubmed |
| pubmed-article:7525297 | pubmed:author | pubmed-author:DayMM | lld:pubmed |
| pubmed-article:7525297 | pubmed:author | pubmed-author:SahiJJ | lld:pubmed |
| pubmed-article:7525297 | pubmed:author | pubmed-author:VohraHH | lld:pubmed |
| pubmed-article:7525297 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7525297 | pubmed:volume | 24 | lld:pubmed |
| pubmed-article:7525297 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7525297 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7525297 | pubmed:pagination | 2618-24 | lld:pubmed |
| pubmed-article:7525297 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:7525297 | pubmed:meshHeading | pubmed-meshheading:7525297-... | lld:pubmed |
| pubmed-article:7525297 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7525297 | pubmed:articleTitle | Macrophage-T cell interaction in experimental mycobacterial infection. Selective regulation of co-stimulatory molecules on Mycobacterium-infected macrophages and its implication in the suppression of cell-mediated immune response. | lld:pubmed |
| pubmed-article:7525297 | pubmed:affiliation | Immunology Lab, Institute of Microbial Technology, Chandigarh, India. | lld:pubmed |
| pubmed-article:7525297 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7525297 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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