Enhanced antigen presenting and T cell functions during late-phase allergic responses in the lung

M. C. Liu, H. Q. Xiao, L. M. Breslin, Bruce Scott Bochner, J. T. Schroeder

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Background: Allergic inflammation is a common feature of asthma and may contribute to both development and perpetuation of disease. The interaction of antigen-presenting cells (APC) with sensitized helper T lymphocytes (TC) producing Th2 cytokines may determine the inflammatory response. Recruitment of APC and TC to the lung during allergic responses has been demonstrated, but functional studies in humans have been limited. Objective: This study examined the function of APC and TC accumulating at sites of inflammation after segmental allergen challenge (SAC). Methods: Fifteen allergic patients underwent SAC, and cells from bronchoalveolar lavage (BAL) were collected after 24 hours. APC and TC from the blood and BAL were purified based on expression of the monocyte marker, CD14; the plasmacytoid dendritic cell (pDC) marker, BDCA4, identifying neuropilin-1 (NRP1); and the helper T cell marker, CD4. Functional activity was assessed using allergen-induced T cell proliferation. Flow cytometry identified cells expressing CD14 and NRP1. Results: SAC resulted in a 12-fold increase in mononuclear cells having the morphologic appearance of blood monocytes. Most of these cells co-expressed CD14 and NRP1. After saline challenge, BAL mononuclear cells demonstrated little APC function. Following SAC, BAL mononuclear cells showed function equal to pDC from blood and greater than blood monocytes. Purified NRP1 + cells from BAL had even greater function than pDC cells from blood (P =.008). Using consistent sources of APC, enhanced proliferation of TC from lung compared to blood was also demonstrated (P =.002). Conclusions: The marked increase in APC function for allergen-specific TC proliferation during allergic inflammation is largely due to the recruitment of monocytes and dendritic cells. There is also an enhanced response in the lung TC population, consistent with recruitment of allergen-specific T cells. Interactions between recruited APC and TC may occur as an early event promoting allergic airway inflammation.

Original languageEnglish (US)
Pages (from-to)334-342
Number of pages9
JournalClinical and Experimental Allergy
Volume48
Issue number3
DOIs
StatePublished - Mar 1 2018

Fingerprint

Antigen-Presenting Cells
Allergens
Neuropilin-1
Bronchoalveolar Lavage
T-Lymphocytes
Lung
Dendritic Cells
Monocytes
Inflammation
Helper-Inducer T-Lymphocytes
Cell Proliferation
Blood Cells
Flow Cytometry
Asthma
Cytokines
Population

Keywords

  • T cells
  • asthma
  • dendritic cells

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Liu, M. C. ; Xiao, H. Q. ; Breslin, L. M. ; Bochner, Bruce Scott ; Schroeder, J. T. / Enhanced antigen presenting and T cell functions during late-phase allergic responses in the lung. In: Clinical and Experimental Allergy. 2018 ; Vol. 48, No. 3. pp. 334-342.
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Enhanced antigen presenting and T cell functions during late-phase allergic responses in the lung. / Liu, M. C.; Xiao, H. Q.; Breslin, L. M.; Bochner, Bruce Scott; Schroeder, J. T.

In: Clinical and Experimental Allergy, Vol. 48, No. 3, 01.03.2018, p. 334-342.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Enhanced antigen presenting and T cell functions during late-phase allergic responses in the lung

AU - Liu, M. C.

AU - Xiao, H. Q.

AU - Breslin, L. M.

AU - Bochner, Bruce Scott

AU - Schroeder, J. T.

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N2 - Background: Allergic inflammation is a common feature of asthma and may contribute to both development and perpetuation of disease. The interaction of antigen-presenting cells (APC) with sensitized helper T lymphocytes (TC) producing Th2 cytokines may determine the inflammatory response. Recruitment of APC and TC to the lung during allergic responses has been demonstrated, but functional studies in humans have been limited. Objective: This study examined the function of APC and TC accumulating at sites of inflammation after segmental allergen challenge (SAC). Methods: Fifteen allergic patients underwent SAC, and cells from bronchoalveolar lavage (BAL) were collected after 24 hours. APC and TC from the blood and BAL were purified based on expression of the monocyte marker, CD14; the plasmacytoid dendritic cell (pDC) marker, BDCA4, identifying neuropilin-1 (NRP1); and the helper T cell marker, CD4. Functional activity was assessed using allergen-induced T cell proliferation. Flow cytometry identified cells expressing CD14 and NRP1. Results: SAC resulted in a 12-fold increase in mononuclear cells having the morphologic appearance of blood monocytes. Most of these cells co-expressed CD14 and NRP1. After saline challenge, BAL mononuclear cells demonstrated little APC function. Following SAC, BAL mononuclear cells showed function equal to pDC from blood and greater than blood monocytes. Purified NRP1 + cells from BAL had even greater function than pDC cells from blood (P =.008). Using consistent sources of APC, enhanced proliferation of TC from lung compared to blood was also demonstrated (P =.002). Conclusions: The marked increase in APC function for allergen-specific TC proliferation during allergic inflammation is largely due to the recruitment of monocytes and dendritic cells. There is also an enhanced response in the lung TC population, consistent with recruitment of allergen-specific T cells. Interactions between recruited APC and TC may occur as an early event promoting allergic airway inflammation.

AB - Background: Allergic inflammation is a common feature of asthma and may contribute to both development and perpetuation of disease. The interaction of antigen-presenting cells (APC) with sensitized helper T lymphocytes (TC) producing Th2 cytokines may determine the inflammatory response. Recruitment of APC and TC to the lung during allergic responses has been demonstrated, but functional studies in humans have been limited. Objective: This study examined the function of APC and TC accumulating at sites of inflammation after segmental allergen challenge (SAC). Methods: Fifteen allergic patients underwent SAC, and cells from bronchoalveolar lavage (BAL) were collected after 24 hours. APC and TC from the blood and BAL were purified based on expression of the monocyte marker, CD14; the plasmacytoid dendritic cell (pDC) marker, BDCA4, identifying neuropilin-1 (NRP1); and the helper T cell marker, CD4. Functional activity was assessed using allergen-induced T cell proliferation. Flow cytometry identified cells expressing CD14 and NRP1. Results: SAC resulted in a 12-fold increase in mononuclear cells having the morphologic appearance of blood monocytes. Most of these cells co-expressed CD14 and NRP1. After saline challenge, BAL mononuclear cells demonstrated little APC function. Following SAC, BAL mononuclear cells showed function equal to pDC from blood and greater than blood monocytes. Purified NRP1 + cells from BAL had even greater function than pDC cells from blood (P =.008). Using consistent sources of APC, enhanced proliferation of TC from lung compared to blood was also demonstrated (P =.002). Conclusions: The marked increase in APC function for allergen-specific TC proliferation during allergic inflammation is largely due to the recruitment of monocytes and dendritic cells. There is also an enhanced response in the lung TC population, consistent with recruitment of allergen-specific T cells. Interactions between recruited APC and TC may occur as an early event promoting allergic airway inflammation.

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KW - asthma

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