T cell responses in allergic rhinitis, asthma and atopic dermatitis

Sustiel, Andrew M.; Rocklin, Ross E.

doi:10.1111/j.1365-2222.1989.tb02337.x

Cited by 47 publications

(13 citation statements)

References 54 publications

(56 reference statements)

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“…In accordance with other studies [9], the ratio of T helper (CD4+) to T cytotoxic (CD8+) cells (CD4/CD8 ratio) was normal in allergic asthmatics. However, in nonallergic asthmatics the CD4/CD8 ra- tio was significantly increased due to decreased num bers of CD8+ T cells.…”

Section: T Lymphocyte Surface Markerssupporting

confidence: 92%

T Cells and Asthma

Walker

Virchow

Bruijnzeel

et al. 1991

Int Arch Allergy Immunol

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Peripheral blood eosinophilia of both allergic and nonallergic asthmatics was found to correlate with blood T cell activation and lymphokine production. A close correlation was shown between the increase of IL-2 receptor expressing T cells and the number of eosinophils. These in vivo activated T cells spontaneously released factors that prolonged eosinophil survival in vitro. The T cell derived lymphokines IL-5, GM-CSF and IL-3 were demonstrated to be responsible for prolonged eosinophil survival in vitro, and were identified in T cell supernatants and sera from asthmatics. In summary, T cell derived cytokines play an important regulatory function towards eosinophils in asthma.

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Section: T Lymphocyte Surface Markerssupporting

confidence: 92%

T Cells and Asthma

Walker

Virchow

Bruijnzeel

et al. 1991

Int Arch Allergy Immunol

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“…In accordance with other studies [7], peripheralblood lymphocyte subpopulations including T cell subsets (CD2+, CD4+, CD8+), B cells and natural killer cells were generally similar between asthmatic patients and normal individuals. However, nonal lergic asthmatics showed a significantly increased CD4/CD8 ratio, resultingfrom decreased numbers of CD8+Tcells ( …”

Section: Lymphocyte Subpopulaiionssupporting

confidence: 92%

T Cells and Asthma

Walker¹,

Virchow²,

Iff³

et al. 1991

Int Arch Allergy Immunol

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Abnormalities of peripheral-blood lymphocyte subsets and activation markers were detected in patients with both allergic and nonallergic asthma. Most allergic asthmatics were characterized by increased numbers of IL-2R⁺ helper T cells and CD23⁺B cells. In contrast, nonallergic asthmatics showed increased numbers of IL-2R⁺ and HLA-DR⁺ helper and cytotoxic T cells, and a clear redistribution from naive (CD45RA⁺) to memory (CD45RO⁺) cells. The number of IL-2R⁺ T cells correlated with the number of CD23⁺ B cells in allergic asthma. These changes in the distribution and activation state of T cells suggest an active role for T cells in the pathogenesis of both allergic and nonallergic asthma.

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“…Effects of ozone exposure on non-IgE-mediated pulmonary hyperimmune reactions that might be induced by Th-1-mediated immune reactions have never been studied. A role for T cells in COPD and asthma is suggested by several authors (Garssen et al, 1991(Garssen et al, , 1994Olaguibel & Basomba, 1989;Sustiel & Rocklin, 1989;Scheerens et al, 1996). On the one hand T cells, in particular Th-2, play a crucial role in the modulation of IgE production.…”

Section: Discussionmentioning

confidence: 97%

Ozone-Induced Impairment of Pulmonary Type Iv Hypersensitivity and Airway Hyperresponsiveness in Mice

Garssen

1997

Inhalation Toxicology

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It is evident that exposure to ozone has toxic effects and can lead to lung function disturbances. Individuals suffering from COPD or asthma are groups especially at risk with respect to the effects of ozone. The majority of studies dealing with ozone effects on pulmonary allergy are restricted to immunoglobulin E ( IgE) mediated allergy ( type I allergy). It has been demonstrated that ozone can potentiate the induction as well as the effector phase of allergic asthma. Recently it has been demonstrated in animal models that in non-IgE-mediated "asthma," T cells may play a role also. It has been demonstrated in mice that low-molecular-weight compounds can induce pulmonary delayed-type hypersensitivitylike reactions that are Th-1 dependent. For this reason it might be suggested that in certain non-IgE-mediated pulmonary diseases Th-1 cells are involved. This in contrast to the classical allergic immune response in asthma where Th-2 cells are thought to be crucial. Effects of ozone on non-IgE-mediated pulmonary allergy induced by, for example, lowmolecular-weight compounds such as toluene diisocyanate, nickel, and trimellitic anhydride have never been studied. In this study we demonstrated that acute ozone exposure can inhibit pulmonary delayed-type hypersensitivity induced by low-molecular-weight compounds in the mouse. The inflammatory component and the hyperresponsiveness of the trachea that is induced by this type of hypersensitivity reaction are significantly inhibited by ambient ozone levels. As is true for the effects on type I allergy, this type of hypersensitivity can also be affected in the induction as well as the effector phase. The results of this study are in general opposite to the effect on type I allergic reactions. The effect, that is, suppression of type IV hypersensitivity, may be due to activation of Th-2 celldependent reactions that may be potentiated by ozone. This potentiation might lead to a downregulation of Th-1-mediated immunity because Th-1 and Th-2 cells modulate each other's activity. On the other hand, it can also be suggested that ozone has a direct effect on Th-1 cells or other cell types that are crucial for delayed-type hypersensitivity and related airway hyperresponsiveness in this animal model.

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T cell responses in allergic rhinitis, asthma and atopic dermatitis

Cited by 47 publications

References 54 publications

T Cells and Asthma

T Cells and Asthma

T Cells and Asthma

Ozone-Induced Impairment of Pulmonary Type Iv Hypersensitivity and Airway Hyperresponsiveness in Mice

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