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Erratum to “control of human host immunity to mycobacteria”
ARTICLE IN PRESS Tuberculosis (2006) 86, 74–75
Tuberculosis http://intl.elsevierhealth.com/journals/tube
ERRATUM
Erratum to ‘‘control of human host immunity to mycobacteria’’ [Tuberculosis 85 (2005) 53–64] Tom H.M. Ottenhoffa,, Frank A.W. Verrecka, Marieke A. Hoevea, Esther vande Vosseb a
Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands b Department of Infectious Diseases, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands
Figure 1 is incorrect (labelling of the key cytokine) and should be replaced with the version below.
DOI of original article: 10.1016/j.tube.2004.09.011
Corresponding author.
E-mail address: [email protected] (T.H.M. Ottenhoff). 1472-9792/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.tube.2005.08.013
ARTICLE IN PRESS Erratum to ‘‘control of human host immunity to mycobacteria’’
STAT3 Jak1 STAT1 IκBα
NEMO IRAK-4 Tyk2 Jak2 STAT4
IL-12R
IFN-α
bacterium
DC-sign Toll/CD14 receptors
β1 β2
IL-12 phagocytosis
IL-27R IL-18R IL-23R
75
IL-27
mannose receptor
IL-18 phagosome
β1 β3
IL-23 IL-15
IL-15R chemokines
bacterial killing IFN-γ TNF-α
T-cell / NK cell
TNF-α
R1 R2
TNF-αR
phagocyte
Figure 1 The type-1 cytokine pathway and its reported, genetic and acquired, deficiencies. IFN-g is produced by type-1 helper T-cells (Th1) and NK-cells and binds to IFN-gR1/R2 receptor complexes on mononuclear phagocytes. Signals from the receptor are transduced by Janus kinases and Stats, particularly Jak-1, Jak-2 and Stat-1. IFN-g, together with TNF-a (which is released by both T-cells and phagocytes), activates microbicidal mechanisms in mononuclear phagocytes, in combination with other factors such as vitamin-D and lymphocytes. Other mechanisms that can contribute to mycobacterial stasis and/or killing include cytolytic granule components such as perforin and granulysin released by cytotoxic T-lymphocytes (CTL), the induction of apoptosis, the presence of ATP, and the activation of Toll-like receptors. Production of IFN-g is regulated by other cytokines, particularly IL-12p70. IL-12 binds to high-affinity IL12Rb1/b2 complexes on Th1- and NK-cells, which signal through IL-12Rb2-associated Stat-4, also involving Jak2, Tyk2, Stat-1, Stat-3 and Stat-5. Similarly, IL-23 signals through IL-23Rb3-associated Stat-3, also involving Tyk2, Jak2, Stat-1 and Stat-4. In addition IL-27, IL-15, IL-18 and possibly other molecules such interferon-a and chemokines are involved in inducing optimal IFN-g production (see text).
Tuberculosis http://intl.elsevierhealth.com/journals/tube
ERRATUM
Erratum to ‘‘control of human host immunity to mycobacteria’’ [Tuberculosis 85 (2005) 53–64] Tom H.M. Ottenhoffa,, Frank A.W. Verrecka, Marieke A. Hoevea, Esther vande Vosseb a
Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands b Department of Infectious Diseases, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands
Figure 1 is incorrect (labelling of the key cytokine) and should be replaced with the version below.
DOI of original article: 10.1016/j.tube.2004.09.011
Corresponding author.
E-mail address: [email protected] (T.H.M. Ottenhoff). 1472-9792/$ - see front matter & 2005 Elsevier Ltd. All rights reserved. doi:10.1016/j.tube.2005.08.013
ARTICLE IN PRESS Erratum to ‘‘control of human host immunity to mycobacteria’’
STAT3 Jak1 STAT1 IκBα
NEMO IRAK-4 Tyk2 Jak2 STAT4
IL-12R
IFN-α
bacterium
DC-sign Toll/CD14 receptors
β1 β2
IL-12 phagocytosis
IL-27R IL-18R IL-23R
75
IL-27
mannose receptor
IL-18 phagosome
β1 β3
IL-23 IL-15
IL-15R chemokines
bacterial killing IFN-γ TNF-α
T-cell / NK cell
TNF-α
R1 R2
TNF-αR
phagocyte
Figure 1 The type-1 cytokine pathway and its reported, genetic and acquired, deficiencies. IFN-g is produced by type-1 helper T-cells (Th1) and NK-cells and binds to IFN-gR1/R2 receptor complexes on mononuclear phagocytes. Signals from the receptor are transduced by Janus kinases and Stats, particularly Jak-1, Jak-2 and Stat-1. IFN-g, together with TNF-a (which is released by both T-cells and phagocytes), activates microbicidal mechanisms in mononuclear phagocytes, in combination with other factors such as vitamin-D and lymphocytes. Other mechanisms that can contribute to mycobacterial stasis and/or killing include cytolytic granule components such as perforin and granulysin released by cytotoxic T-lymphocytes (CTL), the induction of apoptosis, the presence of ATP, and the activation of Toll-like receptors. Production of IFN-g is regulated by other cytokines, particularly IL-12p70. IL-12 binds to high-affinity IL12Rb1/b2 complexes on Th1- and NK-cells, which signal through IL-12Rb2-associated Stat-4, also involving Jak2, Tyk2, Stat-1, Stat-3 and Stat-5. Similarly, IL-23 signals through IL-23Rb3-associated Stat-3, also involving Tyk2, Jak2, Stat-1 and Stat-4. In addition IL-27, IL-15, IL-18 and possibly other molecules such interferon-a and chemokines are involved in inducing optimal IFN-g production (see text).