SidaGhanaV1, Main, Exploration, bibRecord, 001084

Lack of induction of interleukin-2-receptor-α in patients with tuberculosis and human immunodeficiency virus co-infection: implications for pathogenesis

Identifieur interne : 001084 ( Main/Exploration ); précédent : 001083; suivant : 001085

Lack of induction of interleukin-2-receptor-α in patients with tuberculosis and human immunodeficiency virus co-infection: implications for pathogenesis

Auteurs : Stephen D. Lawn [Royaume-Uni, États-Unis] ; Donna Rudolph [États-Unis] ; Alain Ackah [Côte d'Ivoire] ; Doulhourou Coulibaly [Côte d'Ivoire] ; Stefan Wiktor [Côte d'Ivoire] ; Renu B. Lal [États-Unis]

Source :

Transactions of the Royal Society of Tropical Medicine and Hygiene [ 0035-9203 ] ; 2001.

RBID : ISTEX:D5172770E1E1C71A139CCD6BD60DD381FCF09F1B

English descriptors

Abstract

Since expression of both interleukin-2 (IL-2) and IL-2-receptor-α (IL-2R-α) by lymphocytes is inhibited by human immunodeficiency virus (HIV) in vitro, we hypothesized that HIV-co-infection among persons with tuberculosis (TB) might impair T-lymphocyte responses to TB via this mechanism. We measured soluble IL-2R-α (sIL-2R-α), a surrogate marker of T-lymphocyte activation and proliferation, and soluble tumour necrosis factor receptor I (sTNF-RI) in sera from West African patients categorized into 4 groups: those with TB alone (TB+ HIV−, n = 55), CD4-matched groups with TB and HIV co-infection (TB+ HIV+, n = 50) or HIV infection alone (TB− HIV+, n = 35), and patients with neither disease (TB− HIV−, n = 35). The median level of sIL-2R-α was markedly greater in the TB+ HIV− group (1580 U/mL) compared to the TB− HIV− (670 U/mL; P < 0.001) and TB− HIV+ (880 U/mL; P < 0.01) groups. More importantly, the median concentration of sIL-2R-α was much lower in the TB+ HIV+ group (855 U/mL) compared to the TB+ HIV− group (1580 U/mL; P < 0.01) despite similar levels of sTNF-RI. These results suggest that T-lymphocyte activation in TB patients is impaired by HIV co-infection and, furthermore, this suppressive effect was independent of numerical depletion of CD4 lymphocytes. Impairment to IL-2-signalling might contribute to the profound impact that HIV has had on both the incidence and the clinicopathological manifestations of TB.

Url:

https://api.istex.fr/document/D5172770E1E1C71A139CCD6BD60DD381FCF09F1B/fulltext/pdf

DOI: 10.1016/S0035-9203(01)90212-3

Affiliations:

Côte d'Ivoire, Royaume-Uni, États-Unis

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Le document en format XML

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<front><div type="abstract" xml:lang="en">Since expression of both interleukin-2 (IL-2) and IL-2-receptor-α (IL-2R-α) by lymphocytes is inhibited by human immunodeficiency virus (HIV) in vitro, we hypothesized that HIV-co-infection among persons with tuberculosis (TB) might impair T-lymphocyte responses to TB via this mechanism. We measured soluble IL-2R-α (sIL-2R-α), a surrogate marker of T-lymphocyte activation and proliferation, and soluble tumour necrosis factor receptor I (sTNF-RI) in sera from West African patients categorized into 4 groups: those with TB alone (TB+ HIV−, n = 55), CD4-matched groups with TB and HIV co-infection (TB+ HIV+, n = 50) or HIV infection alone (TB− HIV+, n = 35), and patients with neither disease (TB− HIV−, n = 35). The median level of sIL-2R-α was markedly greater in the TB+ HIV− group (1580 U/mL) compared to the TB− HIV− (670 U/mL; P < 0.001) and TB− HIV+ (880 U/mL; P < 0.01) groups. More importantly, the median concentration of sIL-2R-α was much lower in the TB+ HIV+ group (855 U/mL) compared to the TB+ HIV− group (1580 U/mL; P < 0.01) despite similar levels of sTNF-RI. These results suggest that T-lymphocyte activation in TB patients is impaired by HIV co-infection and, furthermore, this suppressive effect was independent of numerical depletion of CD4 lymphocytes. Impairment to IL-2-signalling might contribute to the profound impact that HIV has had on both the incidence and the clinicopathological manifestations of TB.</div>
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Lack of induction of interleukin-2-receptor-α in patients with tuberculosis and human immunodeficiency virus co-infection: implications for pathogenesis

Lack of induction of interleukin-2-receptor-α in patients with tuberculosis and human immunodeficiency virus co-infection: implications for pathogenesis

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

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