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PMID: 6848619 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Possible role for C-reactive protein in the human natural killer cell response.

The Journal of experimental medicine ·Vol. 157 ·No. 1 ·1983-01-01 ·Pages 301-11

Baum LL, James KK, Glaviano RR, Gewurz H

Abstract

Functional NK activity can be removed from human PBL and from phagocyte- and T cell-depleted LGL preparations by treatment with antisera specific for C-reactive protein (CRP) in the presence of complement (C). Pretreatment of NK effector cells with high concentrations of anti-CRP in the absence of C also depletes functional activity. These results indicate that CRP or an antigenically similar molecule is present on a population of NK effector cells. Fluorescent antibody studies in which biotin-avidin amplification was used confirm the presence of surface CRP (S-CRP) on a small percentage of nonphagocytic peripheral blood mononuclear cells. S-CRP readily caps off, which suggest that removal by capping obviates killing by this cell population. This indicates that S-CRP or a molecule that co-caps with S-CRP may be required for successful effector-target cell interaction. The addition of exogenous CRP or CRP-CPS complexes, however, does not alter NK responses. A subpopulation of lymphoid cells responsible for functional NK activity therefore appears to bear surface CRP.

MeSH Terms
C-Reactive Protein/immunology Cell Membrane/immunology Cells, Cultured Complement System Proteins/immunology Cytotoxicity, Immunologic Humans Immunologic Capping Killer Cells, Natural/immunology
Chemicals
Complement System Proteins C-Reactive Protein
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Baum L L
James K K
Glaviano R R
Gewurz H
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19 references, click to expand
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Article Info
Journal
The Journal of experimental medicine
Abbr.
J Exp Med
ISSN
0022-1007
Published
1983-01-01
Pages
301-11
Language
English
Region
United States
NLM ID
2985109R
PMCID
PMC2186896
Subset
IM
Grants
NIAID NIH HHS · AI-12870 · United States
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