Abstract
OX40 is one of the co-stimulatory molecules expressed on T cells, and it is engaged by OX40L, primarily expressed on professional antigen-presenting cells such as dendritic cells. The OX40L–OX40 axis is involved in the sustained activation and expansion of effector T and effector memory T cells, but it is not active in naïve and resting memory T cells. Ligation of OX40 by OX40L accelerates both T helper 1 (Th1) and T helper 2 (Th2) effector cell differentiation. Recent therapeutic success in clinical trials highlights the importance of the OX40L–OX40 axis as a promising target for the treatment of atopic dermatitis.
Highlights
Recent therapeutic success in clinical trials highlights the importance of the OX40L–OX40 axis as a promising target for the treatment of atopic dermatitis
Ligation of OX40 by recombinant OX40L upregulates the expression of interferon-γ and IL-4 in human T cells stimulated with phytohemagglutinin, whereas it downregulates the production of IL-17A [33]
OX40+ dermal cells are co-localized with OX40L+. Cells, such as mast cells in the lesional skin of patients with atopic dermatitis [60]. These results stress that the OX40L–OX40 axis is probably an integral part of the pathogenic T helper 2 (Th2) deviation crucial for atopic dermatitis
Summary
Full T cell activation requires three key signals: engagement of T cell receptors by antigen peptide-bound major histocompatibility complex, ligation of co-stimulatory molecules, and support from cytokines [1]. There are several co-stimulatory and co-inhibitory molecules, known as immune checkpoint molecules (Figure 1). The therapeutic success of blocking antibodies for co-inhibitory molecules, such as programmed cell death 1, programmed death ligand 1, and cytotoxic T lymphocyte-associated protein 4, against melanoma and other cancers supports the multidirectional potential for targeting other immune checkpoint molecules in treating malignancies, autoimmune diseases, and allergic disorders [3,4,6,7,8]. OX40 (TNFRSF4, CD134) and its ligand OX40L (TNFSF4, CD252) are two such TNFSF/TNFRSF co-stimulatory immune checkpoint molecules [10,11].
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