The C-C chemokine receptors CCR4 and CCR8 identify airway T cells of allergen-challenged atopic asthmatics

T Cells of Atopic Asthmatics Preferentially Infiltrate Into Human Bronchial Xenografts in SCID Mice

“…The reason for this gap may be due to the stimulation of the airways by allergen. We did not stimulate the airways by Ag while Panina-Bordignon et al (30) did. In fact, their findings showed that the expressions of IL-4, CCR4, and CCR8 were not observed before allergen exposure to the asthmatics.…”

“…Panina-Bordignon et al (30) demonstrated that, in asthmatics after allergen challenge, T cells in the bronchi express IL-4, CCR4, and CCR8, and that bronchial epithelia express the CCR4-specific ligands monocyte-derived chemokine (MDC) and TARC. These findings suggested that allergic response in the asthmatic airways causes release of MDC and TARC in the epithelium which stimulates Th2-type cells through CCR4 to migrate into the airway tissue where allergic inflammation is ongoing.…”

The chemokine system: tuning and shaping by regulation of receptor expression and coupling in polarized responses

“…In contrast, CCR8 -/-mice were protected against higher airway hyperreactivity. Recent careful analysis of chemokine receptors expressed in T cells in asthma has yielded results consistent with a role of this molecule in allergic inflammation (60). It was found that in allergic asthma CCR3 is rarely expressed in T cells, unlike CCR4 and CCR8.…”

Chemokine Receptor 4 Plays a Key Role in T Cell Recruitment into the Airways of Asthmatic Patients

“…T lymphocytes of the Th2 type (Th2 T cells), driven by chronic exposure to environmental airborne allergens, are increased in asthmatic airways and play a central role in orchestrating this inflammatory response by regulating IgE production, accumulation, and activation of eosinophils, as well as contributing to airway remodeling involving the epithelium and fibroblasts (3,4). The accumulation of Th2 T cells in the lungs is essential for both the initiation and persistence of airway inflammation (3), and studies in asthmatic volunteers have shown marked increases in Th2 T cells in the lungs after in vivo allergen challenge (5). However, the mechanisms by which these cells accumulate within the asthmatic lungs are poorly understood, although a number of candidates, including the chemokine receptors CCR3, CCR4, and CCR8 and the PG D2 receptor CRTH2 (chemoattractant receptor-homologous molecule expressed on Th2 lymphocytes), have been implicated because of their preferential expression on T cells producing Th2 cytokines (6)(7)(8)(9)(10)(11)(12).…”

“…Evidence in human asthma has remained circumstantial, being based on the demonstration that CCR4+ cell counts and the expression of the CCR4 ligands CCL17 and CCL22 increases in the airways after allergen challenge of mild, steroid-naive patients with asthma (5,15,22).…”