Open AccessPollen‐induced antigen presentation by mesenchymal stem cells and T cells from allergic rhinitis
Author(s) -
Desai Mauli B,
Gavrilova Tatyana,
Liu Jianjun,
Patel Shyam A,
Kartan Saritha,
Greco Steven J,
Capitle Eugenio,
Rameshwar Pranela
Publication year - 2013
Publication title -
clinical and translational immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.321
H-Index - 34
ISSN - 2050-0068
DOI - 10.1038/cti.2013.9
Subject(s) - immunology , mesenchymal stem cell , immune system , allergic inflammation , antigen , inflammation , major histocompatibility complex , antigen presentation , allergy , medicine , t cell , pathology
Mesenchymal stem cells (MSCs) are promising cellular suppressor of inflammation. This function of MSCs is partly due to their licensing by inflammatory mediators. In cases with reduced inflammation, MSCs could become immune‐enhancer cells. MSCs can suppress the inflammatory response of antigen‐challenged lymphocytes from allergic asthma. Although allergic rhinitis (AR) is also an inflammatory response, it is unclear if MSCs can exert similar suppression. This study investigated the immune effects (suppressor vs enhancer) of MSCs on allergen‐stimulated lymphocytes from AR subjects (grass or weed allergy). In contrast to subjects with allergic asthma, MSCs caused a significant ( P <0.05) increase in the proliferation of antigen‐challenged lymphocytes from AR subjects. The increase in lymphocyte proliferation was caused by the MSCs presenting the allergens to CD4 + T cells (antigen‐presenting cells (APCs)). This correlated with increased production of inflammatory cytokines from T cells, and increased expressions of major histocompatibility complex (MHC)‐II and CD86 on MSCs. The specificity of APC function was demonstrated in APC assay using MSCs that were knocked down for the master regulator of MHC‐II transcription, CIITA . The difference in the effects of MSCs on allergic asthma and AR could not be explained by the sensitivity to the allergen, based on skin tests. Thus, we deduced that the contrasting immune effects of MSCs for antigen‐challenged lymphocytes on AR and allergic asthma could be disease specific. It is possible that the enhanced inflammation from asthma might be required to license the MSCs to become suppressor cells. This study underscores the need for robust preclinical studies to effectively translate MSCs for any inflammatory disorder.