Cellular immune response to the cell walls of<i>Mycobacterium leprae</i>in leprosy patients and healthy subjects exposed to leprosy

Roche, Paul; Neupane, Kapil Dev; Britton, Warwick J.

doi:10.1111/j.1365-2249.1992.tb06887.x

Cited by 7 publications

(2 citation statements)

References 17 publications

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“…In leprosy, the severity of signs and symptoms depends on the strength of the immune system of the host (Roche et al ., 1992; Andersen et al ., 1994; Ooi & Srinivasan, 2004). The bacteria themselves make little damage since they do not secrete toxins; however, a non‐resistant immune system leads to tissue changes in the body.…”

Section: Osseous Changes In Leprosymentioning

confidence: 99%

Possible cases of leprosy and tuberculosis in medieval Sigtuna, Sweden

Kjellström¹

2010

Intl J of Osteoarchaeology

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In Sigtuna, Sweden, a medieval cemetery, including 227 skeletons, was analysed in 2006. On the outskirts of the churchyard, six skeletons with bone changes indicating systemic inflammatory disease were observed. Two out of three individuals with well-preserved facial bone regions displayed signs of rhinomaxillary remodelling. Four of the afflicted exhibit severe bilateral alterations of the lower legs and phalanges of the feet and concentric atrophy of the metatarsals. In addition, one of the individuals exhibited a kyphosis in the lumbar vertebrae. In a discussion about alternative diagnoses, lepromatous leprosy and tuberculosis were identified as the causes of the destructive lesions in two individuals. Though the skeletal changes of the lower legs and feet in four cases demonstrate a close resemblance to secondary lesions of leprosy, the disease could not be confirmed. The skeletal changes of the last individual were unspecific and the possible causes several, rendering diagnosis difficult. The burial locations imply that the afflicted persons belonged to a lower social stratum. Due to the significantly higher frequency of pathological changes in the cemetery compared to other cemeteries in the town, the individuals could be regarded as fellow sufferers among others with various medical conditions. The bioarchaeological identification of systemic infectious diseases of a group of individuals of this size is unique to Q1 north Q1 of Scania in Sweden, where only a few cases of leprosy and tuberculosis have previously been diagnosed. The significance of the present study is emphasised by the interconnection between the afflicted, the archaeological context and the knowledge of the medieval society in Sigtuna.

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Section: Osseous Changes In Leprosymentioning

confidence: 99%

Possible cases of leprosy and tuberculosis in medieval Sigtuna, Sweden

Kjellström¹

2010

Intl J of Osteoarchaeology

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“…Mycobacterium leprae-spccific T cell clones also recognize epitopes on purified M. leprae cell wall proteins [28,29], the 36-kD proline-rich antigen and a i2-kD protein [30]. The polycional proliferative responses of PBMC to native cell wall proteins parallel the responses to M. leprae across the leprosy spectrum [31], but the identity of these cell wall proteins is unresolved. Therefore although M. leprae-spec\f\c cellular responses have been defined at the epitope level, as yet no single protein has been shown to stimulate M. /epraf-specific responses alone.…”

Section: A3mentioning

confidence: 99%

T cell clones from a non-leprosy exposed subject recognize theMycobacterium leprae18-kD protein

Adams¹,

Basten²,

Prestidge

et al. 1995

Clinical and Experimental Immunology

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SUMMARYAlthough Mycobacterium leprae shares many protein antigens with other mycobacterial species, there is a degree of specificity in the Tcell response to the organism. This is evident in the failure of cross-protection between mycobacterial species and the specific unresponsiveness to M. leprae in lepromatous leprosy patients. The antigenic basis of this specificity is unresolved, but the M. leprae 18-kD protein is one candidate because of its restricted distribution and the isolation of M. Icpraespecific T cell clones reactive with the protein from M. /c/jrac-vaccinated subjects. In the course of analysing the human T cell repertoire to mycobacteria we have isolated further CD4' T cell clones reactive with this protein from a subject who had never been exposed to M. teprae. These clones did not respond to other mycobacteria, including M. tuberculosis and M. bovis (BCG). In addition, they were unrcactive with the M. tuberculosis 16-kD protein which has recently been shown to have limitedaminoacididentity with theA/./('p/w 18-kD protein. Both clones reacted with peptide 38-50 from the M. leprae 18-kD protein, the T cell response to which is restricted by HLA-DR4. Although homologues for the gene encoding the M. leprae 18-kD antigen have been identified in M. avium and M. intracellidarc. the clones failed to respond to preparations of M. uvium. Both clones secreted inlerferon-gamma (IFN-->) and tumour necrosis factor-beta (TNF-/i) and were cytolytic against autologous targets pulsed with peptide 38-50 or the 18-kD protein. The nature of the antigen which stimulates this apparently 'A/. /e/>rae-specific' response is unknown. Nevertheless the recognition of the 18-kD protein by individuals not exposed to leprosy indicates that this protein may not be suitable as a reagent to distinguish between infection with M. teprae and other pathogenic mycobacteria.

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3. Immunology of leprosy

Britton

1993

Transactions of the Royal Society of Tropical Medicine and Hygi

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The host immune response to Mycobacterium leprae is critical for control of the infection but also responsible for the immunopathological damage to skin and nerves. The complex and varied immune responses to the organism are the basis for the clinical spectrum of disease ranging from tuberculoid to lepromatous leprosy. The cellular interactions underlying this spectrum are discussed and the antigenic components of the bacillus briefly reviewed. M. leprae has evolved a variety of mechanisms to avoid macrophage bactericidal mechanisms. These result in the persistence of bacilli and the release of cytokines leading to chronic granulomatous inflammation. The immune response to M. leprae is dynamic and spontaneous variations in cellular reactivity occur with time leading to type I and II leprosy reactions. The factors which preset the host immune response to a tuberculoid or lepromatous pattern and which precipitate reactional episodes remain to be elucidated.

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Cellular immune response to the cell walls ofMycobacterium lepraein leprosy patients and healthy subjects exposed to leprosy

Cited by 7 publications

References 17 publications

Possible cases of leprosy and tuberculosis in medieval Sigtuna, Sweden

Possible cases of leprosy and tuberculosis in medieval Sigtuna, Sweden

T cell clones from a non-leprosy exposed subject recognize theMycobacterium leprae18-kD protein

3. Immunology of leprosy

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