Videos
In this episode, Kelly Singel and colleagues reveal that mature neutrophils acquire a suppressive phenotype in the ovarian cancer microenvironment that is linked to complement C3 activation.
In this episode, Marc Ruitenberg and colleagues demonstrate that complement receptor C3aR stimulates PTEN to inhibit neutrophil-mediated inflammatory pathology following traumatic spinal cord injury.
Antiretroviral therapy (ART) is the standard of care for patients with HIV. For most patients, ART-mediate suppression of HIV replication is accompanied by reconstitution of CD4+ T cells; however, in some cases, the CD4+ T cell population is not fully restored, and these immunological nonresponders (INRs) have increased mortality. In this episode, Irini Sereti, Andrea Lisco, and colleagues identify and characterize immune parameters of 5 patients with a dramatic decline of CD4+ T cells despite ART-mediated viral suppression that is greater than that of subjects with INR. The authors define this condition as extreme immune decline (EXID) and show that it can result from the development of anti–CD4+ T cell autoantibodies and aberrant inflammasome/caspase-1 activation.
The immune system is critical for detecting and eradicating aberrant, tumorigenic cells, and failure of the immunosurveillance system to target these nascent, emerging tumors leads to cancer development. In this episode, Robert Binder and colleagues determined that compared to WT animals, mice lacking the receptor CD91 on antigen-presenting cells are more susceptible to chemical-induced tumor formation as the result of underdeveloped early effector immune responses that in turn enable emergence of neo-antigen-expressing tumors. Moreover, in patients with lung squamous cell carcinomas and skin cutaneous melanomas, CD91 polymorphisms that affect ligand binding associated with poorer immune response. These results indicate that CD91 has potential to predict cancer risk and progression.
Precise control of airway mucin secretion is essential for maintaining proper lung function. In this episode, Burton Dickey, Ana Jaramillo, and colleagues evaluate the role of different isoforms of the scaffolding protein Munc18 in the airway. Munc18a was required for baseline mucin secretion, Munc18b was linked to mucin secretion in response to stimuli, and Munc18c did not contribute to airway mucin secretion. Moreover, Munc18b-deficinet mice showed a reduction of pathogenic phenotypes in multiple models of airway disease, including allergic asthma, cystic fibrosis, and emphysema. These results highlight differences in exocytic machinery at baseline and in response to stimuli that have potential as therapeutic targets.
