Volume 218, Issue 1, October 2024

(A) Minimum spanning tree of eosinophil populations present in the blood of 10 patients with EoE before and after treatment with orodispersible budesonide as well as healthy subjects (HS) determined by X-shift clustering analysis. The sizes of the circles represent the sizes of the populations. The color of the circles indicates the levels of galectin-10, FOXP3, CD16, CD274 (PD-L1), IL-5R, and IL-2R expression as shown by the heat-map scale. Numbers indicate populations that are altered after treatment [1–3 ]. Phenotypes of populations 1–3 are shown below. (B) OPLS-DA was done to see which eosinophil markers could separate EoE patients before and after treatment (n  = 10). (C) Loading plots with jackknife confidence intervals for the eosinophil markers are shown as boxes with ticks. The markers closely positioned to the patient categories are positively associated with the patient category in question. The generated two-component model had an explanatory power of 53% (goodness of fit R2Y = 0.53) and stability of 37% (Q2Y = 0.37).

In this review, Pauzuolis et al. give an overview about the current state of organoids in infection research in the gastrointestinal tract. The review highlights host cellular differentiation, its importance for infection, and how this can be modelled with organoids.

This review discusses the significance of intestinal organoids as a model for studying immune-epithelial interactions in the gut. Organoids replicate key features of native tissues and have advanced our understanding of the immune system’s role in maintaining and regenerating the intestinal barrier during health and disease. The review highlights the various applications of intestinal organoids in immunological research, including co-culturing with immune cells, generating tissue-specific immune cells, and exploring the impact of disease-associated risk genes on the intestinal immune environment.

Potential use and translational applications of patient-derived organoids are very diverse. Such models have revolutionized research in immunological diseases. Co-culture of organoids and immune cells can be used to model diseases, test genetic and environmental factors, and screen drugs or compounds with health-promoting or homeostasis-restoring potentials.

TIM-1 and -3 play distinct roles in autoimmunity, with TIM-1 acting as a costimulatory molecule and TIM-3 regulating Th1 responses. We investigated the therapeutic potential of anti-TIM-1 (RMT1-10) and anti-TIM-3 (RMT3-23) antibodies in an autoimmune arthritis model. An amelioration of autoimmune arthritis was achieved by blocking the TIM-1 and -3 signaling pathways via RMT1-10 and RMT3-23 administration, leading to a widespread decrease in inflammatory cytokines. Both antibodies exhibited therapeutic effects, suggesting TIM-1 and -3 as potential targets for rheumatoid arthritis.

This paper investigates the effect of beta-adrenergic stimulation on human labial minor salivary gland epithelial cells (LMSGEC) on IL-6 production, and its dependency on endoplasmic reticulum (ER) stress. Primary LMSGEC from Sjögren’s syndrome (SS) patients and controls in culture were stimulated with epinephrine and IL-6 expression was evaluated by qPCR and ELISA.

Despite similar IgG antibody levels, adults with overweight/obesity (BMI ≥ 23 kg/m² ) have lower neutralizing antibody capacity and higher T-cell responses to SARS-CoV-2 following COVID-19 recovery. In contrast, antigen-specific antibody and T-cell responses are preserved in individuals with diabetes mellitus who survive SARS-CoV-2 infection.

S100A8/A9 emerges as a valuable marker for monitoring disease activity. Neopterin and S100A8/A9 might help physicians to monitor subclinical inflammation during the attack-free periods of FMF patients. MMP3 might aid in diagnosing FMF attacks when distinguishing between attack and attack-free periods is challenging.

This study highlights the role of Tim-4 in modulating the homeostasis and function of NKT cells during acute liver injury. Tim-4 deficiency enhances IFN-γ, TNF-α expression while impaired IL-4 production in NKT cells and aggravates α-GalCer-inducedliver injury. This study might shed light on the novel role of Tim-4 on NKT cells and identifies Tim-4 as a promising therapeutic target for acute liver inflammatory diseases.