NFAM1 Promotes Pro-Inflammatory Cytokine Production in Mouse and Human Monocytes.
Animals
B-Lymphocytes
/ immunology
CD40 Antigens
/ immunology
CD40 Ligand
/ immunology
Cells, Cultured
Colitis, Ulcerative
/ immunology
Crohn Disease
/ immunology
Cytokines
/ immunology
Humans
Inflammation
/ immunology
Inflammatory Bowel Diseases
/ immunology
Interleukin-12
/ immunology
Intestinal Mucosa
/ immunology
Male
Membrane Proteins
/ immunology
Mice
Mice, Transgenic
Monocytes
/ immunology
Neutrophils
/ immunology
Signal Transduction
/ immunology
T-Lymphocytes
/ immunology
Tumor Necrosis Factor-alpha
/ immunology
B cells
CD40L
Crohn’s disease
NFAM1
inflammation
inflammatory bowel disease
knockout mice
monocytes
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2021
2021
Historique:
received:
09
09
2021
accepted:
13
12
2021
entrez:
31
1
2022
pubmed:
1
2
2022
medline:
25
2
2022
Statut:
epublish
Résumé
NFAT activating protein with ITAM motif 1 (NFAM1) is an ITAM bearing-transmembrane receptor that has been reported to play a role in B cell signaling and development. We performed expression analysis of NFAM1 using publicly available gene expression data sets and found that NFAM1 expression is significantly induced in intestinal biopsies from Crohn's disease (CD) and ulcerative colitis (UC) patients. At the cellular level, we further observed high expression of NFAM1 in monocytes and neutrophils, and low expression in B and T cells. To explore the role of NFAM1 in multiple immune cells and its potential role in IBD, we generated NFAM1
Identifiants
pubmed: 35095847
doi: 10.3389/fimmu.2021.773445
pmc: PMC8793151
doi:
Substances chimiques
CD40 Antigens
0
Cytokines
0
Membrane Proteins
0
NFAM1 protein, human
0
Tumor Necrosis Factor-alpha
0
CD40 Ligand
147205-72-9
Interleukin-12
187348-17-0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
773445Informations de copyright
Copyright © 2022 Juchem, Gounder, Gao, Seccareccia, Yeddula, Huffmaster, Côté-Martin, Fogal, Souza, Wang, Glynn, Yung, Ritchie, Li, Zheng, Mbow, Li and Chanda.
Déclaration de conflit d'intérêts
SC served as Principal Investigator of the contract. KWJ, JPG, ES, ACM, SEF, DS, SSW, ERAG, IY, JR, LL, JZ, MLM and JL were employees of Boehringer Ingelheim. The authors disclose that financial support for this project was provided by Boehringer Ingelheim via a research contract to Sanford Burnham Prebys Medical Discovery Institute. Boehringer Ingelheim had the following involvement with the study: experimental design, data acquisition, analysis and writing the paper.
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