The global response to the COVID-19 pandemic: how have immunology societies contributed?

The COVID-19 pandemic is shining a spotlight on the field of immunology like never before. To appreciate the diverse ways in which immunologists have contributed, Nature Reviews Immunology invited the president of the International Union of Immunological Societies and the presidents of 15 other national immunology societies to discuss how they and their members responded following the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)

The Neutrophil II

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The defensive alliance between neutrophils and NK cells as a novel arm of innate immunity.

The immune system is equipped with a plethora of mechanisms that protect the host from the harmful effects of environmental insults. However, the traditional "hierarchical" view of the immune response, in which innate, "nonspecific" cells are first recruited to the site of damage, before the highly "specific", adaptive immune response develops, has been questioned recently. First, the innate response is much more specific than recognized previously: indeed, each cell of the innate system is not only endowed with an ever-expanding array of germ-line-encoded receptors, which differentiate between distinct insults, but also is modulated continuously by other leukocytes that concomitantly interact with and respond to that particular insult. The other reason is that the cells of the innate system are instrumental for the adaptive system to accomplish its function, as they can also modulate the activity of lymphocytes reciprocally during the entire course of the immune response. This complex pattern of interactions is illustrated by recent advances on the functions of PMNs, clearly showing that unexpectedly, these cells also contribute to the regulation of the host immune response by crosstalk with innate and adaptive leukocytes, including NK cells. Herein, given the peculiar role of neutrophils and NK cells in inflammation, clearance of pathogens/viral-infected cells, and cancer immunosurveillance, we summarize the current knowledge about the mechanisms whereby neutrophils and NK cells interact and regulate the activities of one another, as well as discuss their potential implications involved in the pathogenesis of chronic, inflammatory pathologies, infections, and tumors

Myeloid cells, BAFF and IFNg establish an inflammatory loop that exacerbates autoimmunity in Lyn-deficient mice

In this study we demonstrate that the reciprocal production of BAFF and IFNg establishes an inflammatory loop between myeloid cells and T cells that exacerbates autoimmunity in the Lyn-deficient model of autoimmunity. Our findings uncover an important pathological role of BAFF in autoimmune disorders

B cell-derived IL-10 suppresses inflammatory disease in Lyn-deficient mice.

These data reveal a dominant immunosuppressive function of B cell-derived IL-10 in the Lyn-deficient model of autoimmunity, extending our current understanding of the role of IL-10 and IL-10-producing B cells in SL

On the co-purification of 6-sulfo LacNAc(+) dendritic cells (slanDC) with NK cells enriched from human blood.

The ability of NK cells to directly recognize pathogens and be activated via Toll-like receptors (TLR) is increasingly recognized. Nevertheless, controversial results on the NK cell ability to be directly activated by lipopolysaccharide (LPS), the ligand of TLR4, have been recently reported. To start elucidating the reasons explaining the contrasting observations of the literature, we focused on the potential role of currently used NK cell purification procedures to condition putative NK cell responsiveness to LPS. To do so, human NK cells were isolated by negative selection, using three different commercial kits, to be comparatively evaluated for the production of IFN\u3b3 in response to ultra-pure LPS and/or IL-2. Despite the lack of surface TLR4, we found that two out of the three NK cell-enriched populations released IFN\u3b3 (and one of the two, IL-12p70 as well) in response to the LPS plus IL-2 combination, whereas the last one did not. However, the two LPS plus IL-2-responsive NK cell populations were found variably contaminated with 6-sulfo LacNAc+ dendritic cells (slanDC), demonstrated responsible for triggering, via the production of IL-12p70 in response to LPS, the release of IFN\u3b3 by IL-2-stimulated NK cells. Accordingly, slanDC depletion completely abrogated the capacity to produce both IL-12p70 and IFN\u3b3 in response to LPS plus IL-2 by slanDC-containing NK cells. Taken together, our data uncover that two commercially available kits, specifically designed to isolate NK cells by negative selection, also co-purify variable amounts of slanDC. The latter cells may dramatically affect the outcome of experiments carried on to evaluate NK cell responsiveness to TLR agonists such as LPS