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Partial body cryotherapy (PBC) is proposed to alleviate symptoms of exercise-induced muscle damage (EIMD) by reducing associated inflammation. No studies have assessed acute PBC exposure on peripheral blood mononuclear cell mobilisation or compared these with cold water immersion (CWI), which may inform how PBC impacts inflammatory processes. This trial examined the impact of a single PBC exposure on circulating peripheral blood mononuclear cells compared to CWI or a control. 26 males were randomised into either PBC (3 min at − 110 to − 140 °C), CWI (3 min at 9 °C), or control (3 min at 24 °C), with blood samples, heart rate, and blood pressure taken before and after exposure. Cytometric analysis determined that CD8+ T-cell populations were significantly elevated after treatments, with PBC increasing CD8+ T cells to a greater degree than either CWI or CON. Natural killer cell counts were also elevated after PBC, with the increase attributed specifically to the CD56loCD16+ cytotoxic subset. This provides the first evidence for the effect of PBC exposure on redistribution of immune cells. An increase in circulating leukocyte subsets such as CD8+ T cells and CD56loCD16+ natural killer cells suggests that PBC may induce a transient mobilisation of lymphocytes. PBC may thus enable a more efficient trafficking of these cells from the circulation to the site of initial cellular insult from exercise, potentially accelerating the process of cellular recovery. This provides novel evidence on the use of PBC as a recovery treatment and may also have applicability in other clinical settings involving the recovery of damaged skeletal muscle. [ABSTRACT FROM AUTHOR]

The given name and family names of five author were incorrectly structured. The correct given name and family names should be: Helen McGuire. Correction to: Partial body cryotherapy exposure drives acute redistribution of circulating lymphocytes: preliminary findings. [Extracted from the article]

Type 2 immunity is critical for defense against cutaneous infections but also underlies the development of allergic skin diseases. We report the identification in normal mouse dermis of an abundant, phenotypically unique group 2 innate lymphoid cell (ILC2) subset that depended on interleukin 7 (IL-7) and constitutively produced IL-13. Intravital multiphoton microscopy showed that dermal ILC2 cells specifically interacted with mast cells, whose function was suppressed by IL-13. Treatment of mice deficient in recombination-activating gene 1 (Rag1−/−) with IL-2 resulted in the population expansion of activated, IL-5-producing dermal ILC2 cells, which led to spontaneous dermatitis characterized by eosinophil infiltrates and activated mast cells. Our data show that ILC2 cells have both pro- and anti-inflammatory properties and identify a previously unknown interactive pathway between two innate populations of cells of the immune system linked to type 2 immunity and allergic diseases. [ABSTRACT FROM AUTHOR]

Dendritic cells (DCs) within the skin are a heterogeneous population of cells, including Langerhans cells of the epidermis and at least three subsets of dermal DCs. Collectively, these DCs play important roles in the initiation of adaptive immune responses following antigen challenge of the skin as well as being mediators of tolerance to self-antigen. A key functional aspect of cutaneous DCs is their migration both within the skin and into lymphatic vessels, resulting in their emigration to draining lymph nodes. Here, we discuss our current understanding of the requirements for successful DC migration in and from the skin, and introduce some of the microscopic techniques developed in our laboratory to facilitate a better understanding of this process. In particular, we detail our current use of multi-photon excitation (MPE) microscopy of murine skin to dissect the migratory behavior of DCs in vivo. [ABSTRACT FROM AUTHOR]

The mammalian immune system has an extraordinary potential for making receptors that sense and neutralize any chemical entity entering the body. Inevitably, some of these receptors recognize components of our own body, and so cellular mechanisms have evolved to control the activity of these‘forbidden’ receptors and achieve immunological self tolerance. Many of the genes and proteins involved are conserved between humans and other mammals. This provides the bridge between clinical studies and mechanisms defined in experimental animals to understand how sets of gene products coordinate self-tolerance mechanisms and how defects in these controls lead to autoimmune disease. [ABSTRACT FROM AUTHOR]