Graphical abstract and Figures of review named A New Perspective: Systemic Immunity from Tears

I.Data type: jpgII. Contents: 1.Graphical abstract，2.Figure 1III. Figure captions which explained the contents and meanings of the figures including the meanings of abbreviations.1.Graphical abstract—— ocular immune mechanisms of systemic diseasesIn conditions like Sjögren's syndrome (SS), Rheumatoid arthritis (RA), Systemic lupus erythematosus (SLE), Multiple sclerosis (MuS), Alzheimer's disease (AD), Graves' ophthalmopathy (GO), Diabetes mellitus (DM), and Coronavirus disease-19 (COVID-19), various immunopathological mechanisms manifest as inflammation on the ocular surface. Tears have a diverse array of resident immune cells. As these diseases advance, both the cellular population ratios and the cytokine profiles—including IL-2, IL-4, IL-6, IL-8, IFN-γ and TGF-β—undergo dynamic shifts. GVHD: graft-versus-host disease; SLE: lupus erythematosus; GO: Graves' ophthalmopathy; MuS: multiple sclerosis; SS: Sjögren syndrome; RA: rheumatoid arthritis; COVID: coronavirus disease-19; AD: Alzheimer’s disease; DM: diabetes mellitus; INF: interferon; TNF: tumor necrosis factor; TGF: transforming growth factor; IFN: Interferon.2.Figure1: The physiological immune mechanism in tearsVarious immune cells partake in ocular inflammatory reactions. Tear neutrophils attract Th17 cells via the production of CCL2 and CCL20, respectively binding to CCR2 and CCR6 for action. Neutrophils can induce IL-17a; their self-activation is mediated by the IL-17 receptor (IL-17RC). These neutrophils decelerate T cell responses and exert immunosuppressive impacts through interactions involving CD11B (Mac-1). Epithelial cells in the lacrimal gland releasing type IgA instigate local immune activation, exhibiting both pro-inflammatory and anti-inflammatory capabilities. IgA engages with CD71, initiating an inflammatory feedback loop by enhancing its expression. IgA modulates human Th17-type cells, foundational contributors to numerous inflammatory and allergic conditions. IgA can impede the differentiation, proliferation, and secretion of their effector cytokine, IL-17A, from human Th17-type cells as well as inhibit IFN-γ responses. IL: interleukin; CCL: C-C motif chemokine; CCR: C-C Chemokine Receptors; CD: Cluster of Differentiation; TCR: T Cell Receptor; Tfh: T follicular helper cells; Th: T helper cells; IL-17RC: Interleukin-17 Receptor Cell; IgA: Immunoglobulin; MHC II: Major Histocompatibility Complex IIIV.Both of the figures are made by Adobe Illustrator 2021-2022