Journal
JOURNAL OF IMMUNOLOGY
Volume 167, Issue 5, Pages 2651-2656Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.167.5.2651
Keywords
-
Categories
Funding
- NIAID NIH HHS [AI42127, AI41530, AI65299] Funding Source: Medline
- NIDCR NIH HHS [DE72621, DE09691, DE08228] Funding Source: Medline
- NIDDK NIH HHS [DK47322, DK34151, DK54495] Funding Source: Medline
Ask authors/readers for more resources
The intestinal mucosa normally displays minimal inflammation despite the close proximity between mucosal macrophages and lumenal bacteria. Macrophages interact with bacteria and their products through CD14, a surface receptor involved in the response to LPS, and CD89, the receptor for IgA (Fc alphaR). Here we show that resident macrophages isolated from normal human intestine lack CD14 and CD89. The absence of CD14 and CD89 was not due to the isolation procedure or mucosal cell products, but was evident at the transcriptional level, as the macrophages expressed neither CD14(-) nor CD89-specific mRNAs, but did express Toll-like receptor 2 and 4 transcripts. Consistent with their CD14(-) phenotype, lamina propria macrophages displayed markedly reduced LPS-induced cytokine production and LPS-enhanced phagocytosis. In addition, IgA-enhanced phagocytosis was sharply reduced in lamina propria macrophages. Thus, the absence of CD14 and CD89 on resident intestinal macrophages, due to down-regulated gene transcription, causes down-modulated LPS- and IgA-mediated functions and probably contributes to the low level of inflammation in normal human intestinal mucosa.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available