Fate of T Cells and their Secretory Proteins During the Progression of Leprosy
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Leprosy is an infectious disease caused by non-cultivable bacteria Mycobacterium leprae. Ridley and Jopling classified the disease into five polar forms, Tuberculoid (TT) and Lepromatous (LL), in between two forms of the disease Borderline tuberculoid (BT), Borderline (BB) and Borderline lepromatous (BL) are laid. The tuberculoid type (BT/TT) leprosy patients show good recall of cellmediated immune (CMI) response and Th1 type of immune response, while lepromatous leprosy (LL) patients show defect in cell-mediated immunity to the causative agent and Th2 type of immune response. Due to distinct clinical and immunological spectra of the disease, leprosy attracted immunologists to consider an ideal model for the study of deregulations of various immune reactions. Recent studies show that Tregs, Th3 (TGF-β, IL-10), IL-35 producing Treg immune response associated with the immune suppressive environment, survival of bugs. IL-17 producing Th17 immune response associated with tuberculoid leprosy and play protective role. γδ T cells also increased from tuberculoid to lepromatous pole of leprosy. In this review, we will discuss the role of various subtypes of T-cell and their cytokines in the pathogenesis of leprosy. Keywords: Leprosy, Th1 and Th2 cells, Treg cells, pathogenesis of leprosy, tuberculoid leprosy, cytokines.Keywords:
Tuberculoid leprosy
Mycobacterium leprae
Pathogenesis
Mycobacterium leprae
Tuberculoid leprosy
Intracellular parasite
Cellular immunity
Cell mediated immunity
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This paper discusses the evidence for and against the view that the spectrum of pathological changes in leprosy, extending from the lepromatous form to the tuberculoid form, may be caused by differences in the immune responses of patients. Patients with the tuberculoid form of leprosy generally have well-developed specific cell-mediated immunity, but in a large proportion of patients with lepromatous leprosy the specific cell-mediated immunity to Mycobacterium leprae and sometimes to other antigens seems to be deficient, whereas the circulating antibody response is well-developed. Techniques for assessing the immune response in patients are described in detail with the objective of improving the comparability of such investigations. The paper also discusses the importance of several investigatory approaches to clinical leprosy and the value of animal models for leprosy research.
Mycobacterium leprae
Tuberculoid leprosy
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Leprosy is an infectious disease caused by non-cultivable bacteria Mycobacterium leprae. Ridley and Jopling classified the disease into five polar forms, Tuberculoid (TT) and Lepromatous (LL), in between two forms of the disease Borderline tuberculoid (BT), Borderline (BB) and Borderline lepromatous (BL) are laid. The tuberculoid type (BT/TT) leprosy patients show good recall of cellmediated immune (CMI) response and Th1 type of immune response, while lepromatous leprosy (LL) patients show defect in cell-mediated immunity to the causative agent and Th2 type of immune response. Due to distinct clinical and immunological spectra of the disease, leprosy attracted immunologists to consider an ideal model for the study of deregulations of various immune reactions. Recent studies show that Tregs, Th3 (TGF-β, IL-10), IL-35 producing Treg immune response associated with the immune suppressive environment, survival of bugs. IL-17 producing Th17 immune response associated with tuberculoid leprosy and play protective role. γδ T cells also increased from tuberculoid to lepromatous pole of leprosy. In this review, we will discuss the role of various subtypes of T-cell and their cytokines in the pathogenesis of leprosy. Keywords: Leprosy, Th1 and Th2 cells, Treg cells, pathogenesis of leprosy, tuberculoid leprosy, cytokines.
Tuberculoid leprosy
Mycobacterium leprae
Pathogenesis
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Journal Article 3. Immunology of leprosy Get access Warwick J. Britton Warwick J. Britton Department of Medicine, University of Sydney (Do6), Sydney 2006, Australia Search for other works by this author on: Oxford Academic PubMed Google Scholar Transactions of The Royal Society of Tropical Medicine and Hygiene, Volume 87, Issue 5, September 1993, Pages 508–514, https://doi.org/10.1016/0035-9203(93)90066-Y Published: 01 September 1993
Tropical Medicine
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Mycobacterium leprae
Tuberculoid leprosy
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Leprosy is a chronic inflammatory disease caused by Mycobacterium leprae. The human response to this pathogen exhibits intriguing aspects which are up to now not well understood. The present study discusses the probable mechanisms involved in T cell-specific unresponsiveness observed in lepromatous patients. Analysis of the cytokine profile either in blood leukocytes or in skin specimens taken from leprosy lesions indicates that some parameters of Th1 immune response are present in lepromatous patients under reactional states
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A large number of organisms such as viruses, protozoa, helminths, fungi and bacteria, especially mycobacteria, need cell-mediated immunological processes for their elimination. As well as being involved in protection, cell-mediated immunological processes are also involved in a number of allergic reactions to products derived from mycobacteria. Cell-mediated immunological processes can be demonstrated by a number of in vitro reactions. Leprosy can present with a wide range of different clinical patterns. The clinical spectrum of leprosy can be shown to depend on the degree of the cell-mediated immune response of the host against Mycobacterium leprae. Thus in tuberculoid leprosy there is a high degree of cell-mediated immune response whereas in lepromatous leprosy such a response is virtually absent. There appears to be a constitutional predisposition to lepromatous leprosy. In addition to a specific loss of cell-mediated immune response against Myco. leprae, there is also a non-specific drop in the ability of patients with lepromatous leprosy to show other aspects of cell-mediated immune response, e.g., contact sensitivity and skin homograft rejection. There is also a relative impairment of the ability of lymphocytes to react in vitro. Lymph nodes from patients with lepromatous leprosy show a deficiency in those areas associated with the development of cell-mediated immune responses.The article includes a discussion on the possible causes of deficiencies in cell-mediated immune responses in lepromatous leprosy.
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Cell-mediated immunity or hypersensitivity to M. leprae and other unrelated antigens, such as tuberculin and dinitrochlorobenzene, was studied in 73 leprosy patients of different histopathologic types. It was found that specific as well as nonspecific anergy intensified as the disease spectrum shifted from the tuberculoid toward the lepromatous immunologic pole. Within the lepromatous group, the impairment of cellular immunity became more pronounced as the bacillary load increased. It was found that the impairment of the cell-mediated immunity towards antigens other than M. leprae became more severe as the duration of the illness increased. Late lepromin responsiveness, which is the hallmark of resistance of an individual to M. leprae, may be absent even before the onset of clinical illness. Its deficit seems to be primary and has a genetic predisposition.
Mycobacterium leprae
Cellular immunity
Delayed hypersensitivity
Genetic predisposition
Tuberculoid leprosy
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Mycobacterium leprae
Tuberculoid leprosy
T helper cell
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Immunological responsiveness was studied throughout the clinical and histopathological spectrum of leprosy (Ridley–Jopling scale) by the methods of lymphocyte transformation, leucocyte migration inhibition and delayed skin hypersensitivity,
The response to Mycobacterium leprae showed by all methods a continuous decrease from strong responses in the polar tuberculoid (TT) group to virtually negative responses in the polar lepromatous (LL) group. There was a good agreement between the in vitro methods and the lepromin skin test, giving support to the latter as useful tool in the evaluation of immune responsiveness to M. leprae in leprosy patients.
The immune response to BCG and PPD on the other hand, decreased only slightly towards the lepromatous pole of the spectrum, confirming the high degree of specificity of the immune defect in lepromatous leprosy. Patients grouped histologically as subpolar tuberculoid (TT/BT) reacted particularly strongly to BCG and PPD.
As it is likely that the methods used mainly measured T-lymphocyte function, the clinicopathological manifestations of leprosy appear to reflect the strength of the cellular immune response against M. leprae. Thus the findings give strong support to the concept of a host-determined, immunological diseases pectrum as expressed in the Ridley–Jopling classification.
Mycobacterium leprae
Tuberculoid leprosy
Delayed hypersensitivity
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