Severe Mycobacterial and Salmonella Infections in Interleukin-12 Receptor-Deficient Patients-Reference-Cited by-同舟云学术

Severe Mycobacterial and Salmonella Infections in Interleukin-12 Receptor-Deficient Patients

Published:1998-05-29 Issue:5368 Volume:280 Page:1435-1438
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Jong Rolien de¹²³⁴⁵,Altare Frédéric¹²³⁴⁵,Haagen Inez-Anne¹²³⁴⁵,Elferink Diënne G.¹²³⁴⁵,Boer Tjitske de¹²³⁴⁵,van Breda Vriesman Peter J. C.¹²³⁴⁵,Kabel Peter J.¹²³⁴⁵,Draaisma Johannes M. T.¹²³⁴⁵,van Dissel Jaap T.¹²³⁴⁵,Kroon Frank P.¹²³⁴⁵,Casanova Jean-Laurent¹²³⁴⁵,Ottenhoff Tom H. M.¹²³⁴⁵

Affiliation:

1. R. de Jong, D. G. Elferink, T. de Boer, T. H. M. Ottenhoff, Department of Immunohematology and Bloodbank, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, the Netherlands.

2. F. Altare and J-L. Casanova, INSERM Unité 429, Hôpital Necker-Enfants Malades,149, Rue de Sevres, 75743 Paris Cedez 15, France.

3. I.-A. Haagen and P. J. C. van Breda Vriesman, Department of Immunology, University Hospital Maastricht, P.O. Box 5800, 6202 AZ Maastricht, the Netherlands.

4. P. J. Kabel and J. M. T. Draaisma, Department of Medical Microbiology and Immunology, and Department of Pediatrics, St. Elisabeth Hospital, P.O. Box 747, 5000 AS Tilburg, the Netherlands.

5. J. T. van Dissel and F. P. Kroon, Department of Infectious Diseases, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, the Netherlands.

Abstract

Interleukin-12 (IL-12) is a cytokine that promotes cell-mediated immunity to intracellular pathogens by inducing type 1 helper T cell (T H 1) responses and interferon-γ (IFN-γ) production. IL-12 binds to high-affinity β1/β2 heterodimeric IL-12 receptor (IL-12R) complexes on T cell and natural killer cells. Three unrelated individuals with severe, idiopathic mycobacterial and S almonella infections were found to lack IL-12Rβ1 chain expression. Their cells were deficient in IL-12R signaling and IFN-γ production, and their remaining T cell responses were independent of endogenous IL-12. IL-12Rβ1 sequence analysis revealed genetic mutations that resulted in premature stop codons in the extracellular domain. The lack of IL-12Rβ1 expression results in a human immunodeficiency and shows the essential role of IL-12 in resistance to infections due to intracellular bacteria.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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