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Adipose Tissue Macrophages Function As Antigen-Presenting Cells and Regulate Adipose Tissue CD4+ T Cells in Mice
- Source :
- Diabetes
- Publication Year :
- 2013
- Publisher :
- American Diabetes Association, 2013.
-
Abstract
- The proinflammatory activation of leukocytes in adipose tissue contributes to metabolic disease. How crosstalk between immune cells initiates and sustains adipose tissue inflammation remains an unresolved question. We have examined the hypothesis that adipose tissue macrophages (ATMs) interact with and regulate the function of T cells. Dietary obesity was shown to activate the proliferation of effector memory CD4+ T cells in adipose tissue. Our studies further demonstrate that ATMs are functional antigen-presenting cells that promote the proliferation of interferon-γ–producing CD4+ T cells in adipose tissue. ATMs from lean and obese visceral fat process and present major histocompatibility complex (MHC) class II–restricted antigens. ATMs were sufficient to promote proliferation and interferon-γ production from antigen-specific CD4+ T cells in vitro and in vivo. Diet-induced obesity increased the expression of MHC II and T-cell costimulatory molecules on ATMs in visceral fat, which correlated with an induction of T-cell proliferation in that depot. Collectively, these data indicate that ATMs provide a functional link between the innate and adaptive immune systems within visceral fat in mice.
- Subjects :
- CD4-Positive T-Lymphocytes
medicine.medical_specialty
Endocrinology, Diabetes and Metabolism
Adipose tissue macrophages
Antigen-Presenting Cells
Adipose tissue
Inflammation
Major histocompatibility complex
03 medical and health sciences
0302 clinical medicine
Immune system
Antigen
Internal medicine
Internal Medicine
medicine
Animals
Obesity
Antigen-presenting cell
Original Research
030304 developmental biology
0303 health sciences
biology
Macrophages
3T3-L1
Cell biology
Endocrinology
Adipose Tissue
030220 oncology & carcinogenesis
biology.protein
medicine.symptom
Obesity Studies
Subjects
Details
- ISSN :
- 1939327X and 00121797
- Volume :
- 62
- Database :
- OpenAIRE
- Journal :
- Diabetes
- Accession number :
- edsair.doi.dedup.....bdbd80d16782bf8e8fb7987537e0202b
- Full Text :
- https://doi.org/10.2337/db12-1404