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HERO ID
5369703
Reference Type
Journal Article
Title
QUANTITATIVE DINITROCHLOROBENZENE (DNCB) RESPONSIVITY AND PHYTOHEMAGGLUTININ (PHA) INDUCED LYMPHOCYTE-TRANSFORMATION IN PATIENTS WITH LEPROMATOUS LEPROSY
Author(s)
Rea, TH; Quismorio, F; Harding, B; Friou, G; Levan, N
Year
1976
Is Peer Reviewed?
Yes
Journal
International Journal of Leprosy and Other Mycobacterial Diseases
ISSN:
0148-916X
EISSN:
1544-581X
Publisher
INT JOURNAL LEPROSY
Location
GREENVILLE
Volume
44
Issue
1-2
Page Numbers
250-255
Language
English
PMID
945239
Web of Science Id
WOS:A1976BS28100043
Abstract
Because the authors are unable to find a gross generalized impairment of cell mediated immunity (CMI) in patients with lepromatous leprosy, and because such impairment is evidently readily demonstrated by others, they have sought evidence of a subtle deficit in CMI by quantitating in vivo DNCB and in vitro PHA responses. The subjects of this study were 31 Mexican born patients, who, by the criteria of Ridley and Waters are clinically classified as LL because of an abundance of bacilli in lesions and the absence of borderline lesions, reversal reactions and nerve trunk neuropathies. Responses to DNCB were similar in leprosy patients and in normal controls. PHA induced lymphocyte transformation with fetal bovine serum was also similar in controls and leprosy patients and in subgroups of leprosy patients. This study provided no evidence that a subtle, generalized deficit of CMI is present in this group of patients. A subtle generalized defect of CMI cannot be excluded absolutely and the authors are continuing this investigation utilizing smaller quantities of DNCB and lower dilutions of PHA. Since generalized deficiencies of CMI are not necessary accompaniments of leprosy, their existence must be attributable to a variable other than lepromatous leprosy itself. The authors do not know the responsible variable or variables but possibilities to which the present study is directed include disease extent, presence or absence of sulfone therapy, and LIB (antigen load).
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