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This document defines the inputs and processes used to calibrate the raw images returned by the Didymocs Reconnaissance and Asteroid Camera for OpNav (DRACO) instrument flown aboard the Double Asteroid Redirection Test (DART) mission.

Type 2 immunity is associated with adipose tissue (AT) homeostasis and infection with parasitic helminths, but whether AT participates in immunity to these parasites is unknown. We found that the fat content of mesenteric AT (mAT) declined in mice during infection with a gut-restricted helminth. This was associated with the accumulation of metabolically activated, interleukin-33 (IL-33), thymic stromal lymphopoietin (TSLP), and extracellular matrix (ECM)–producing stromal cells. These cells shared transcriptional features, including the expression of Dpp4 and Pi16 , with multipotent progenitor cells (MPC) that have been identified in numerous tissues and are reported to be capable of differentiating into fibroblasts and adipocytes. Concomitantly, mAT became infiltrated with resident T helper 2 (T H 2) cells that responded to TSLP and IL-33 by producing stromal cell–stimulating cytokines, including transforming growth factor β1 (TGFβ 1 ) and amphiregulin. These T H 2 cells expressed genes previously associated with type 2 innate lymphoid cells (ILC2), including Nmur1 , Calca , Klrg1 , and Arg1 , and persisted in mAT for at least 11 months after anthelmintic drug–mediated clearance of infection. We found that MPC and T H 2 cells localized to ECM-rich interstitial spaces that appeared shared between mesenteric lymph node, mAT, and intestine. Stromal cell expression of epidermal growth factor receptor (EGFR), the receptor for amphiregulin, was required for immunity to infection. Our findings point to the importance of MPC and T H 2 cell interactions within the interstitium in orchestrating AT remodeling and immunity to an intestinal infection.

Type 2 immunity is associated with adipose tissue (AT) homeostasis and infection with parasitic helminths, but whether AT participates in immunity to these parasites is unknown. We found that the fat content of mesenteric AT (mAT) declined in mice during infection with a gut-restricted helminth. This was associated with the accumulation of metabolically activated, interleukin-33 (IL-33), thymic stromal lymphopoietin (TSLP), and extracellular matrix (ECM)-producing stromal cells. These cells shared transcriptional features, including the expression of

Infection with helminth parasites can affect adiposity, but underlying mechanisms that regulate this process are unclear. We found that fat content of mesenteric adipose tissue (mAT) declined in mice during infection with gut-restricted parasitic worms. This was associated with the accumulation of metabolically activated, immunostimulatory cytokine- and extracellular matrix-secreting multipotent stromal cells, which had potential to differentiate into preadipocytes. Concomitantly, mAT became infiltrated with Th2 lymphocytes that took up long-term residence and responded to signals from stromal cells by producing stromal cell-stimulating cytokines, including Amphiregulin. Signals delivered by Amphiregulin to stromal cells were required for immunity to infection. Our findings reveal intricate intercellular communication between Th2 cells and adipocyte progenitors and link immunity to intestinal infection to T cell-dependent effects on the adipocyte lineage.

This document defines the inputs and processes used to calibrate the raw images returned by the Didymocs Reconnaisance and Asteroid Camera for OpNav (DRACO) instrument flown aboard the Double Asteroid Redirection Test (DART) mission.