Universität zu Köln

Dold, L., Zimmer, L., Schwarze-Zander, C., Boesecke, C., Mohr, R., Wasmuth, J. -C., Ommer, K., Gathof, B., Kraemer, B., Nattermann, J., Strassburg, C. P., Rockstroh, J. K., Spengler, U. and Langhans, B. (2021). TLR agonists enhance responsiveness of inflammatory innate immune cells in HLA-B*57-positive HIV patients. J. Mol. Med., 99 (1). S. 147 - 159. HEIDELBERG: SPRINGER HEIDELBERG. ISSN 1432-1440

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Abstract

HLA-B*57 affects the course of HIV infection. Under antiretroviral therapy, its effects cannot be explained by outstandingly efficient T cell responses alone but may also involve cells of innate immunity. Studying in vitro stimulation with Pam3CSK4, E. coli LPS-B5 and CpG-ODN-2216, we observed greater induction of IL-6/IL-1beta double-positive CD14(+)CD16(++) monocytes as well as IFN-gamma-positive cytotoxic CD56(high)CD16(neg) NK cells in HLA-B*57- versus HLA-B*44-positive HIV patients, while TNF-alpha induction remained unchanged. Differences were not seen in the other monocyte and NK cell subsets or in HLA-matched healthy controls. Our findings show that, in virally suppressed HIV infection, HLA-B*57 is associated with enhanced responsiveness of inflammatory innate immune cells to TLR ligands, possibly contributing to increased vulnerability in sepsis. Key messages center dot HLA-B*57 is a host factor affecting clinical outcomes of HIV infection. center dot HLA-B*57 modifies inflammatory subsets of NK cells and monocytes in HIV infection. center dot In HLA-B*57-positive HIV patients TLR agonists induce enhanced IL-6/IL-1beta in monocytes. center dot NK cells from HLA-B*57 HIV patients release more IFN-gamma upon TLR costimulation. center dot HLA-B*57 is linked to enhanced inflammatory responsiveness to TLR ligands.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Dold, L. UNSPECIFIED UNSPECIFIED UNSPECIFIED Zimmer, L. UNSPECIFIED UNSPECIFIED UNSPECIFIED Schwarze-Zander, C. UNSPECIFIED UNSPECIFIED UNSPECIFIED Boesecke, C. UNSPECIFIED UNSPECIFIED UNSPECIFIED Mohr, R. UNSPECIFIED UNSPECIFIED UNSPECIFIED Wasmuth, J. -C. UNSPECIFIED UNSPECIFIED UNSPECIFIED Ommer, K. UNSPECIFIED UNSPECIFIED UNSPECIFIED Gathof, B. UNSPECIFIED UNSPECIFIED UNSPECIFIED Kraemer, B. UNSPECIFIED UNSPECIFIED UNSPECIFIED Nattermann, J. UNSPECIFIED UNSPECIFIED UNSPECIFIED Strassburg, C. P. UNSPECIFIED UNSPECIFIED UNSPECIFIED Rockstroh, J. K. UNSPECIFIED UNSPECIFIED UNSPECIFIED Spengler, U. UNSPECIFIED UNSPECIFIED UNSPECIFIED Langhans, B. UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-308620
DOI:	10.1007/s00109-020-01996-7
Journal or Publication Title:	J. Mol. Med.
Volume:	99
Number:	1
Page Range:	S. 147 - 159
Date:	2021
Publisher:	SPRINGER HEIDELBERG
Place of Publication:	HEIDELBERG
ISSN:	1432-1440
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language NATURAL-KILLER; CLASS-I; COAGULATION; ACTIVATION; RESPONSES; MARKERS Multiple languages Genetics & Heredity; Medicine, Research & Experimental Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/30862