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Allergy. 2019 May 11. doi: 10.1111/all.13867. [Epub ahead of print]

Modulation of CRTh2 expression on allergen-specific T cells following peptide immunotherapy.

Author information

1
Department of Medicine, Division of Clinical Immunology & Allergy, McMaster University, Hamilton, Ontario, Canada.
2
Benaroya Research Institute at Virginia Mason, Seattle, Washington.
3
Department of Medicine, Division of Respirology, Firestone Institute for Respiratory Health, The Research Institute at St. Joe's, Hamilton, Ontario, Canada.

Abstract

BACKGROUND:

Allergen immunotherapy using synthetic peptide T-cell epitopes (Cat-PAD) from the major cat allergen Fel d 1 has been shown, in allergen exposure studies, to significantly reduce symptoms of allergic rhinoconjunctivitis in cat-allergic subjects. However, the immunological mechanisms underlying clinical benefit remain only partially understood. Since previous studies of whole allergen immunotherapy demonstrated a reduction in the frequency of allergen-specific (MHC II tetramer+ ) CD4+ T cells expressing the chemokine receptor CRTh2, we assessed the impact of Cat-PAD on the frequency and functional phenotype of Fel d 1-specific CD4+ T cells.

METHODS:

Using before and after treatment samples from subjects enrolled in a randomized, double-blind, placebo-controlled trial of Cat-PAD, we employed Fel d 1 MHC II tetramers and flow cytometry to analyze the expression of chemokine receptors CCR3, CCR4, CCR5, CXCR3, and CRTh2, together with markers of memory phenotype (CD27 and CCR7) on Fel d 1-specific CD4+ T cells.

RESULTS:

No statistically significant change in the frequency of Fel d 1-specific CD4+ T cells, nor in their expression of chemokine receptors or memory phenotype, was observed. However, a significant reduction in cell surface expression of CRTh2 was observed between the placebo and active groups (P = 0.047).

CONCLUSIONS:

Peptide immunotherapy with Cat-PAD does not significantly alter the frequency or phenotype of Fel d 1-CD4+ T cells, but may decrease their expression of CRTh2.

KEYWORDS:

T cells; chemokines; immunotherapy and tolerance induction; immunotherapy vaccines and mechanisms; vaccines

PMID:
31077596
DOI:
10.1111/all.13867

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