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T J Birdi

Publications and source records attributed to T J Birdi.

29 records · Page 2Linked to original sources
PubMed1985

Mycobacterium leprae-induced alterations in macrophage Fc receptor expression and monocyte-lymphocyte interaction in familial contacts of leprosy patients.

Macrophage Fc receptor expression and monocyte-lymphocyte interaction in the presence of Mycobacterium leprae were examined in familial contacts of leprosy patients. Defective M phi functions similar to those of borderline and lepromatous patients could be observed in approximately 71% of consanguineous contacts and 43% of spouses of index patients. Although the values in the latter group were markedly lower than those of the consanguineous contacts, they tended to be higher than those of normal individuals (20%). These in vitro M phi functions were independent of age, sex, and age at onset of exposure and were only weakly associated with duration of exposure. The outcome of the monocyte-lymphocyte interaction test paralleled to a large extent the in vivo Mitsuda lepromin response. Four contacts with defective M phi functions also showed signs of leprosy. The value of these in vitro tests as markers of 'susceptibility' could therefore prove significant.

Age Factors↗
PubMed1984

In vitro studies on the effect of levamisole in lepromatous leprosy.

Our previous studies have demonstrated a defective macrophage response to M. leprae in lepromatous leprosy patients. In the present study we report the restoration of Fc receptor and HLA-DR antigen expression as well as antigen specific macrophage-lymphocyte interaction on treatment with levamisole in vitro. These results indicate that levamisole activates the macrophages which in turn results in an improved cell mediated immune response in lepromatous leprosy. This may also be applicable in other disease situations.

HLA-DR Antigens↗
PubMed1984

Antigen specific macrophage-lymphocyte interaction in lepromatous leprosy.

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.

Antigens, Bacterial↗
PubMed1984

Mechanism of immunosuppression in leprosy--macrophage membrane alterations.

L-Lysate induced macrophage membrane alteration was studied using 3 membrane markers: (i) Fc receptor, (ii) Concanavalin A (Con A) receptor, and (iii) M. leprae adherence to macrophage membrane. The data indicate that L-lysate induces membrane perturbation of normal macrophages. The alteration can be reversed with trypsin and colchicine. Membrane alteration observed may lead to defective macrophage participation in a cell-mediated immune reaction.

Cell Membrane↗
PubMed1983

Alterations in the membrane of macrophages from leprosy patients.

Macrophage cultures pulsed with viable Mycobacterium leprae were assessed for erythrocyte rosetting in three groups of individuals, i.e., normal subjects, and tuberculoid and lepromatous patients. Of these, only the lepromatous group showed a reduction in rosetting ability after infection with M. leprae. The specificity of such a reduction pattern was confirmed by using various mycobacteria to infect the macrophages. A threshold effect was noted in all three groups. Although a reduction was obtained in the amount of rosetting of macrophages from lepromatous patients with 10(4) acid-fast bacilli per culture, tuberculoid and normal macrophages resisted such an effect with as large a dose as 20 X 10(6) to 30 X 10(6) and 30 X 10(6) bacilli per culture, respectively. The M. leprae-caused alterations in macrophages from lepromatous patients were reversible by treatment with trypsin and colchicine. Cytochalasin B and Tween 80 were unable to alter the pattern. Treatment of cells with neuraminidase was inconclusive since it enhanced rosetting values of both control and infected cultures. These manipulations were significant in elucidating the target point of the host (macrophage) and parasite (M. leprae) interaction and in delineation of the external and internal effects upon the macrophages. Both M. leprae and macrophages were participants in Fc reduction, as treatment of the former with rifampicin and of the latter with cyclocheximide significantly augmented the rosetting ability. In conclusion, it appears that M. leprae, upon entering a lepromatous macrophage, initiates the production of a protein which acts via the microtubules to alter membrane topography. It is possible that the altered membrane prevents effective macrophage-lymphocyte interaction. This could be one of the mechanisms by which cell-mediated immunity is suppressed in lepromatous leprosy.

Animals↗
PubMed1980

Role of macrophages in defective cell mediated immunity in lepromatous leprosy. II. Macrophage and lymphocyte interaction.

Macrophages from lepromatous patients after phagocytosis of M. leprae showed alteration in their surface property as determined by their ability to express Fc receptors. The same macrophages without intracellular M. leprae show normal Fc receptors. The lepromatous macrophages also show very poor interaction with lymphocytes in the presence of M. leprae while they are able to interact with lymphocytes when exposed to other antigens. These observations along with earlier ones on macrophage defects have indicated a probable reason for defective cell mediated immunity (CMI) in lepromatous leprosy patients. There appears to be a defective macrophage population in lepromatous patients that is unable to process M. leprae antigens and initiate the CMI response.

Humans↗
PubMed1980

Role of macrophages in defective cell mediated immunity in lepromatous leprosy. I. Factor(s) from macrophages affecting protein synthesis and lymphocyte transformation.

Macrophages from lepromatous leprosy patients specifically show reduced protein synthesis in the presence of M. leprae. They also produce, as a result of interaction with M. leprae, factor(s) that reduce protein synthesis in normal macrophages as well as block lymphocyte transformation in normal leukocyte cultures in the presence of M. leprae as the antigen. These observations implicate a defective macrophage system in lepromatous leprosy patients.

Cells, Cultured↗
PubMed1979

The role of macrophages in leprosy as studied by protein synthesis of macrophages from resistant and susceptible hosts--a mouse and human study.

3H-leucine uptake by macrophages from swiss white and C57BL mice before and after M. leprae infection was studied. A depression in 3H-leucine uptake after infection was observed only in swiss white mice. 3H-leucine uptake was also studied in blood derived macrophages from normals, and LL and TT patients. A depression was obtained in 3H-leucine uptake after M. leprae infection in macrophages from LL patients.

Animals↗
PubMedDate not supplied

Effect of T-cell depletion on bacterial multiplication and pattern of nerve damage in M. leprae-infected mice.

Various mechanisms for nerve damage in tuberculoid leprosy have been proposed. A common feature amongst them is the crucial role played by T-cells. Therefore, the present study was designed to determine the role of T-cells in the induction of nerve damage in leprosy using two different protocols for obtaining graded levels of T-cell depletion: (i) Cyclosporine A, for depletion of T-helper cells and (ii) Anti Thy 1.2, for total depletion of T-cells. The findings indicate that the early changes seen in the unmyelinated fibres may not involve T-cells. However, the later stages of nerve damage associated with demyelination are dependent on T-cell responses.

Animals↗