immune response

Sarcoptic mange in wild caprinae of the Alps. Could pathology help in filling the gaps in knowledge?

Sarcoptic mange represents the most severe disease for wild Caprinae individuals and populations in Europe, rising concerns for both conservation and management of these ungulates. To date, this disease has been investigated in different wild caprine species and under many different perspectives including diagnostics, epidemiology, impact on the host populations and genetics of both hosts and parasite, with the aim to disentangle the host-Sarcoptes scabiei relationship. Notwithstanding, uncertainty still remains and basic questions still need an answer.

Electrochemotherapy in head and neck cancer: a review of an emerging cancer treatment

Patients affected by aggressive neoplasms with a high propensity to metastasize to the skin, such as some head and neck cancers, can benefit from electrochemotherapy, a modality that combines electroporation of cell membranes and chemotherapy to facilitate the transport of non-permeant molecules into cells; the host immune response consequently participates in achieving cure of tumors.

AMBRA1 Controls Regulatory T-Cell Differentiation and Homeostasis Upstream of the FOXO3-FOXP3 Axis

Regulatory T cells (T reg ) are necessary to maintain immunological tolerance and are key players in the control of autoimmune disease susceptibility. Expression of the transcription factor FOXP3 is essential for differentiation of T reg cells and indispensable for their suppressive function. However, there is still a lack of knowledge about the mechanisms underlying its regulation. Here, we demonstrate that pro-autophagy protein AMBRA1 is also a key modulator of T cells, regulating the complex network that leads to human T reg differentiation and maintenance.

Neuroinflammatory targets and treatments for epilepsy validated in experimental models

A large body of evidence that has accumulated over the past decade strongly supports the role of inflammation in the pathophysiology of human epilepsy. Specific inflammatory molecules and pathways have been identified that influence various pathologic outcomes in different experimental models of epilepsy. Most importantly, the same inflammatory pathways have also been found in surgically resected brain tissue from patients with treatment-resistant epilepsy. New antiseizure therapies may be derived from these novel potential targets.

The Use of Both Therapeutic and Prophylactic Vaccines in the Therapy of Papillomavirus Disease

Human papillomavirus (HPV) is the most common sexually transmitted virus. The high-risk HPV types (i.e., HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59) are considered to be the main etiological agents of genital tract cancers, such as cervical, vulvar, vaginal, penile, and anal cancers, and of a subset of head and neck cancers. Three prophylactic HPV vaccines are available that are bivalent (vs. HPV16, 18), tetravalent (vs. HPV6, 11, 16, 18), and non-avalent (vs. HPV6, 11, 16, 18, 31, 33,45, 52, 58).

Bone Marrow NK Cells: Origin, Distinctive Features, and Requirements for Tissue Localization

NK cell maturation is a continuous process, which initiates in the bone marrow and proceeds in peripheral tissues, where NK cells follow distinct differentiation routes. Drastic phenotypic changes are observed during progression from precursors to mature NK cells, including changes of expression and functionalities of several chemoattractant receptors. Upon differentiation, mature NK cells migrate outside the bone marrow; as well, peculiar subsets of NK cells can also home back to or localize in this anatomic compartment to play specific functions.

John Cunningham virus: an overview on biology and disease of the etiological agent of the progressive multifocal leukoencephalopathy.

John Cunningham virus (JCV), the etiological agent of progressive multifocal leukoencephalopathy
(PML), is the first human polyomavirus described. After asymptomatic primary infection which occurs in
childhood, the virus spreads by the hematogenous route from the primary site of infection to secondary
sites including kidneys, lymphoid tissues, peripheral blood leukocytes, and brain to establish latent infection.
During immunosuppression the virus undergoes molecular rearrangements that allow it to replicate
in glial tissues causing PML.

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