Fcε Receptor II/CD23 Positive Lymphocytes in Atopic Dermatitis: II. Infiltration of FcεR II(+) T cells in the Skin Lesion

Sakamoto, Taiko; Takigawa, Masaharu; Tamamori, T.; Horiguchi, Daisuke; Yamada, Miki

doi:10.1111/1523-1747.ep12505589

Cited by 13 publications

(13 citation statements)

References 20 publications

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“…Either IL-4 or IFN-y can increase the ex pression of membrane-bound or soluble CD23 by Langcrhans cells [21,27]. Interestingly, IL-4 appears to be more effective at increasing expression of membrane-bound CD23, while IFN-y more strongly increases production of soluble CD23 [27], These complex interactions between IL-4, IFN, and CD23 may be important in certain disease states. For ex ample, high levels of IgE and other alterations in immuni ty are seen in many parasitic diseases.…”

mentioning

confidence: 99%

Regulation of the Low Affinity IgE Fc Receptor (CD23) in Atopic Dermatitis

Halpern¹,

Schwartz²

1993

Int Arch Allergy Immunol

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Alterations in the production of CD23, the IgE Fc receptor, may play a role in the etiology of atopic dermatitis and other allergic conditions. Interleukin-4 (IL-4), interferon-γ (IFN-γ), and interferon-α (IFN-α) are involved in coordinate regulation of CD23. IL-4 stimulates production of both CD23 and IgE. IFN-γ also stimulates production of CD23, but suppresses production of IgE and inhibits IL-4-mediated production of CD23. IFN-α also suppresses these IL-4-mediated activities and, in addition, suppresses IFN-γ-mediated stimulation of CD23 production. Changes in this coordinate regulation may be involved in the development of atopic dermatitis. Expression of CD23 by Langerhans cells is stimulated by IL-4 and IFN-γ. Further, levels of CD23-positive T cells are elevated in atopic dermatitis subjects as compared to non-atopic controls, and observed skin changes appear to be related to changes in CD23-positive mononuclear cell populations. Coordinate regulation of CD23 by IFN-γ and IL-4 may also be important in other allergic conditions, parasitic infections, and a variety of disease states.

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confidence: 99%

Regulation of the Low Affinity IgE Fc Receptor (CD23) in Atopic Dermatitis

Halpern¹,

Schwartz²

1993

Int Arch Allergy Immunol

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“…By immunofiuorescent staining the allergen locates on LC partly via IgE bound to FCERII at these sites [40]. Sakamoto et al [24] have found apposition of T cells to FCERII + non-T cells, presumably maerophages in the dermal infiltrate of atopie dermatitis. Environmental allergen may be presented in a way to select T cells with abnormal profiles of cytokine production at skin lesions of atopic dermatitis.…”

Section: Discussionmentioning

confidence: 99%

“…The assumption that an allergenspecific inflammation occurs in atopic lesions [36] predicts an overwhelming number of CD4+ TE cells in the lesions. The preferential appearance of CD8+ TE cells in the peripheral blood and skin lesion in atopic dermatitis [23,24] suggests the concomitant occurrence of polyclonal activation of inflammatory cells partly by IL-4 produced by allergen-specific T cells. Furthermore, as demonstrated by Paliard et al [47], it is possible that IL-4 induces CD8 on CD4+ TE cells, resulting in the enhanced generation of CD8+ TE cells.…”

Section: Discussionmentioning

confidence: 99%

“…We have reported that CD8 is expressed on TE cells in the peripheral blood of patients with severe atopic dermatitis and the acutely exacerbated skin lesion [23,24]. In PBMC cultured with rIL-4 for 3 days both CD4+ and CD8+ TE cells were generated in all groups (Table 4).…”

Section: Suhsets Of Te Cellsmentioning

confidence: 98%

“…Low affinity Fc receptor for IgE (FCERII/CD23) is expressed on several haematopoietic cells including lymphocytes, monocytes/ macrophages, Langerhans cells (LC), platelets and eosinophils [1][2][3][4], It is reported that FCERII is involved in B cell growth and differentiation [5], regulates IgE synthesis by B cells [6][7][8], participates in parasite killing by eosinophils [9], and plays a role in antigen focusing on B cells and LC [10,11], Soluble products of FceRII, known as IgE-binding factor (BF), promote the proliferation of activated B cells and regulate IgE synthesis by IL-4-stimulated peripheral blood cells and B cells from atopic donors [12,13], Thus, FceRII functions in a variety of ways depending on the cell type that expresses it, FCERII expression is regulated by cytokines, IL-4 induces over-expression of FCERII on T and B cells, monocytes and LC, FCERII expression on T cells induced by mitogen and allergen is Correspondence: Masahiro Takigawa, MD, Department of Dermatology, Hamamatsu University School of Medicine, Hamamatsu 431-31, Japan, enhanced in the presence of IL-4 [14][15][16], On the other hand, interferon-gamma (IFN-y) inhibits the expression on IL-4-stimulated T and B cells [ 17,18], whereas monocytes and LC are stimulated to express FCERII by IFN-y [4,13,19], IFN-a suppresses FCERII expression on B cells, monocytes and LC [20], Patients with atopic dermatitis have various humoral and cell-mediated immune dysfunctions [21,22], We have shown that the proportion of FCERII+ lymphocytes in the peripheral blood correlates with the extent of atopic dermatitis, whereas such correlation is not observed in patients with eczematous dermatitis [23], FCERII+ lymphocytes from patients with extensive atopic dermatitis contain TE cells that preferentially express CD8, TE cells are detected among inflammatory cells of atopic dermatitis, and acute skin lesions are infiltrated by CD8+ T« cells [24], Therefore, a critical question is whether FCERII expression on T cells, especially on those with CD8, is intrinsic to atopic lymphocytes following stimulation or secondary to abnormal production of stimuli that induce FCERII,…”

Section: Introductionmentioning

confidence: 99%

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Fcε receptor II/CD23+ lymphocytes in atopic dermatitis. III. Aberrant control in thein vitroexpression of FcεRII/CD23 on peripheral blood T cells in atopic dermatitis

Sakamoto

Nakayama

Tamamori

et al. 1992

Clinical and Experimental Immunology

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SUMMARYIn vitro FCERII expression was examined in patients with atopic dermatitis, those with non-atopic eczematous dermatitis and normal individuals following stimulation of peripheral blood cells with recombinant IL-4 (rIL-4), phytohaemagglutinin (PHA), or PHA plus rIL-2, At various days cells were stained with MoAbs to human lymphocyte FcsRII and to lymphoid cell-surface antigens and analysed by flow cytometry, rIL-4, but not rIL-2, specifically induced FCERII on T cells as well as B cells in atopic dermatitis, eczematous dermatitis and normal individual groups. Both atopies and non-atopies generated comparable proportions of FceRII"*" T cells (Ts cells), whereas the frequency of B cells bearing Fc£RII(B£ cells) was significantly higher in patients with extensive atopic dermatitis than in those with mild atopic dermatitis and other subjects. Comparable levels of Ts cells were detected in both atopic and non-atopic donors following stimulation of peripheral blood cells with PHA or pre-activation ofthe cells with PHA plus subsequent incubation with rIL-2, Whereas both CD8+ and CD4+ subsets were present in Te cell populations induced specifically by rIL-4, PHA and PHA plus rIL-2, patients with atopic dermatitis had a greater tendency for FCERII expression on 008"*" T cells compared with patients with eczematous dermatitis and normal individuals, Recombinant interferon-gamma (rIFN-y), but not rIFN-a or prostaglandin E2 (PGE2), suppressed the generation of TE cells by rIL-4 in atopies and non-atopies to the same degree. These results suggest the aberrant control of FCERII expression on T cells, especially those bearing CD8, in atopic dermatitis.

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