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Helminths are multicellular parasites that are a substantial problem for both human and veterinary medicine. According to estimates, 1.5 billion people suffer from their infection, resulting in decreased life quality and burdens for healthcare systems. On the other hand, these infections may alleviate autoimmune diseases and allergy symptoms. The immune system is programmed to combat infections; nevertheless, its effector mechanisms may result in immunopathologies and exacerbate clinical symptoms. This review summarizes the role of the immune response against worms, with an emphasis on the Th2 response, which is a hallmark of helminth infections. We characterize non-immune cells (enteric tuft cells—ETCs) responsible for detecting parasites, as well as the role of hematopoietic-derived cells (macrophages, basophils, eosinophils, neutrophils, innate lymphoid cells group 2—ILC2s, mast cells, T cells, and B cells) in initiating and sustaining the immune response, as well as the functions they play in granulomas. The aim of this paper is to review the existing knowledge regarding the immune response against helminths, to attempt to decipher the interactions between cells engaged in the response, and to indicate the gaps in the current knowledge. [ABSTRACT FROM AUTHOR]

This article focuses on abstracts of papers presented at the 32nd annual meeting of the American Society of Dermatopathology at Intercontinental Hotel, New Orleans between February 1-3, 1995. The Kveim-Siltzbach Reactions (KSR) is an important model for investigating immunologic events in granuloma formation. It has been shown that T lymphocyte predominance with oligocionality of infiltrating cells in 4 week-old KSR. Verruciform xanthoma is a rare benign condition that commonly involves the oral mucosa. Cutaneous lesions are less often observed, predominantly occurring at anogenital sites. Despite anecdotal reports of its occurrence in a variety of disease states, the etiology of this condition remains unclear.

The regulators of Gprotein signaling (RGS) protein superfamily negatively controls Gprotein-coupled receptor signal transduction pathways. RGS16 is enriched in activated/effector T lymphocytes. In this paper, we show that RGS16 constrains pulmonary inflammation by regulating chemokine-induced T cell trafficking in response to challenge with Schistosoma mansoni. Naive Rgsl6-/- mice were "primed" for inflammation by accumulation of CCR10+ T cells in the lung. Upon pathogen exposure, these mice developed more robust granulomatous lung fibrosis than wild-type counterparts. Distinct Th2 or putative Thl7 subsets expressing CCR4 or CCR10 accumulated more rapidly in Rgsl6-/- lungs following challenge and produced proinflammatory cytokines IL-13 and IL-17B. CCRA+Rgsl6-/- Th2 cells migrated excessively to CCL17 and localized aberrantly in challenged lungs. T lymphocytes were partially excluded from lung granulomas in Rgsl6-/- mice, instead forming peribronchial/perivascular aggregates. Thus, RGS16-mediated confinement of T cells to Schistosome granulomas mitigates widespread cytokine-mediated pulmonary inflammation. [ABSTRACT FROM AUTHOR]

Monogenic autoinflammatory syndromes comprise disorders caused by mutations of different genes encoding for proteins that play a major role in the inflammatory response. They are characterized by seemingly unprovoked inflammatory episodes lacking high concentrations of autoantibodies or autoreactive T cells. The clinical spectrum of these syndromes are extremely variable and is represented by: recurrent fever episodes of variable duration (periodic/recurrent fever), skin lesions (cryopyrinopathies), noncaseating granulomas (granulomatous disorders) and, rarely, by sterile pyogen abscesses (pyogenic disorders). This paper represents a briefly presentation of these disorders. [ABSTRACT FROM AUTHOR]

A conference paper on the role of apoptosis inhibitor expressed by macrophages (AIM) in Corynebacterium-induced granuloma formation in mice is presented. Results reveal the poor repopulation of natural killer T (NKT) cells in middle and late stages of granuloma formation in AIM-/-mice. Apoptosis of NKT cells and T cells was more prominent in AIM-/- mice. These findings indicate that AIM regulates NKT and T cell apoptosis and recruitment and plays a vital role in granuloma formation.