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Cytokine release syndrome (CRS) is a significant side effect associated with chimeric antigen receptor (CAR)-T cell therapy for cancer. CAR-T cells engineered to secrete cytokine modulators can reduce CRS-related toxicity while simultaneously improving in vivo antitumor efficacy.

Schmitt, Duval, et al. show that TL1A is an epithelial cytokine that cooperates with IL-33 in the initiation of allergic airway inflammation. Similar to IL-33, TL1A functions as an alarmin important for early induction of IL-9high ILC2s after allergen exposure.

CD4+ T cells exhibit pleiotropic roles in autoimmunity and cancer. Lalle et al. demonstrate that their function is selectively controlled by different NF-κB subunits depending on the disease context. This work unravels critical regulators of T cell function and paves the way toward NF-κB subunit–targeted immunotherapies.

Midnolin is an essential gene with previously unknown effects in vivo. This paper shows that midnolin stimulates proteasome activity necessary for lymphopoiesis and B cell cancer growth in mice.

SARS-CoV-2 cell tropism and infection cycle are defined at the cellular resolution by infection of healthy human lung tissue and single-cell profiling. Interstitial macrophages are a dominant target of viral takeover, inflammation, and destruction in COVID-19 initiation, and use DC-SIGN/CD209, but not ACE2, for entry.

Horesh et al. use forward and reverse genetics to identify four novel gain-of-function JAK1 mutations in 59 patients. These individuals present with autoimmunity, atopy, colitis, and/or dermatitis, suggestive of a novel syndrome termed JAK1-associated atopy colitis and/or dermatitis (JAACD).

Brief Definitive Report

This study identifies a novel dominant negative heterozygous mutation in OTULIN (p.Cys129S). C129S OTULIN promotes accumulation of linear ubiquitin chains on diverse substrates including LUBAC, causing enhanced cell death and inflammatory signaling, and thereby this heterozygous mutation drives autoinflammatory disease.

Technical Advances and Resources

The poor prognosis of M3 uveal melanomas generates a local adaptive immune response, which does not recirculate, while the better prognosis of SF3B1-mutated uveal melanomas induces a systemic immune response in the absence of a detectable local response.


In this issue, Schmitt et al. identify TNF-like protein 1A (TL1A) as an epithelial alarmin constitutively expressed by a subset of lung epithelial cells, which is released in response to airborne microbial challenge and synergizes with IL-33 to drive allergic disease.

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