Journal of the American Academy of Dermatology · 1997
T-cell cytokine network in cutaneous lupus erythematosus.
Клиническое исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Stein L F, Saed G M, Fivenson D P
Аннотация
BACKGROUND: A variety of immunologic abnormalities have been described in systemic and experimental lupus erythematosus (LE). Several T-cell defects, especially in helper T (Th) cell cytokines, have been reported.
OBJECTIVE: Our purpose was to identify the Th cytokine profile in cutaneous LE.
METHOD: Total RNA was extracted from punch biopsy specimens from 19 patients with cutaneous LE (nine, discoid LE; two, subacute cutaneous LE; and eight, systemic LE) and from four healthy control subjects. RNA was reverse transcribed into complementary DNA and amplified with polymerase chain reaction (PCR) primers specific for interleukin-2 (IL-2), IL-4, IL-5, IL-10, interferon gamma (IFN-gamma), and beta actin. PCR products were detected by agarose gel electrophoresis and Southern blot with 32P-labeled, nested probes.
RESULTS: Sixteen of 19 cutaneous LE specimens lacked IL-2, all were negative for IL-4, and 10 of 19 had detectable IL-10, whereas IFN-gamma and IL-5 messenger RNAs were present in the majority of LE specimens. IFN-gamma and IL-10 mRNAs were found in all normal skin controls, whereas IL-2, IL-4, and IL-5 mRNAs were undetectable. Functional IFN-gamma protein was evidenced by intercellular adhesion molecule-1 and HLA-DR staining of keratinocytes in nine of nine LE specimens but not in normal skin. The pattern of cytokine mRNAs, intercellular adhesion molecule-1, and/or HLA-DR expression in cutaneous LE specimens did not vary with different subtypes of LE, antinuclear antibody titer, or the magnitude of inflammation.
CONCLUSION: The presence of IL-5 mRNA in cutaneous LE specimens suggests that Th type 2 cells combine with local IFN-gamma production to augment disease and may be related to the pathophysiology of cutaneous LE.
OBJECTIVE: Our purpose was to identify the Th cytokine profile in cutaneous LE.
METHOD: Total RNA was extracted from punch biopsy specimens from 19 patients with cutaneous LE (nine, discoid LE; two, subacute cutaneous LE; and eight, systemic LE) and from four healthy control subjects. RNA was reverse transcribed into complementary DNA and amplified with polymerase chain reaction (PCR) primers specific for interleukin-2 (IL-2), IL-4, IL-5, IL-10, interferon gamma (IFN-gamma), and beta actin. PCR products were detected by agarose gel electrophoresis and Southern blot with 32P-labeled, nested probes.
RESULTS: Sixteen of 19 cutaneous LE specimens lacked IL-2, all were negative for IL-4, and 10 of 19 had detectable IL-10, whereas IFN-gamma and IL-5 messenger RNAs were present in the majority of LE specimens. IFN-gamma and IL-10 mRNAs were found in all normal skin controls, whereas IL-2, IL-4, and IL-5 mRNAs were undetectable. Functional IFN-gamma protein was evidenced by intercellular adhesion molecule-1 and HLA-DR staining of keratinocytes in nine of nine LE specimens but not in normal skin. The pattern of cytokine mRNAs, intercellular adhesion molecule-1, and/or HLA-DR expression in cutaneous LE specimens did not vary with different subtypes of LE, antinuclear antibody titer, or the magnitude of inflammation.
CONCLUSION: The presence of IL-5 mRNA in cutaneous LE specimens suggests that Th type 2 cells combine with local IFN-gamma production to augment disease and may be related to the pathophysiology of cutaneous LE.