"We're going to have to cut loose some of our personal beliefs": barriers and opportunities in providing HIV prevention to African American men who have sex with men and women

In the United States, there is an urgent need to provide HIV prevention services to African American men who have sex with men and women (MSMW) but who do not identify as gay or homosexual. Engaging these men in HIV prevention has historically been challenging. This study used qualitative methodology to explore the beliefs and experiences from community-based service providers (n = 21) and from African American MSMW (n = 21) regarding the provision of HIV prevention education and counseling to these men. Data analysis revealed that (a) African American MSMW who do not identify as gay can challenge service providers' assumptions about sexual behavior and sexual identity; (b) service providers' attitudes toward these men can be affected by ambivalent or negative beliefs that pervade the general community; (c) African American MSMW need safe and nonjudgmental spaces that offer HIV risk reduction, but they also might experience anxiety about disclosing same-sex behaviors to counselors. Findings highlighted the complexities related to culture, masculinity, and sexuality as determinants of HIV risk in African American MSMW, and findings also revealed tensions between these factors that may affect the quality of HIV prevention services. Service providers may need additional training to provide appropriate and non-judgmental HIV prevention counseling and education.     

B cell homeostasis and plasma cell homing controlled by Krüppel-like factor 2

Krüppel-like factor 2 (KLF2) controls T lymphocyte egress from lymphoid organs by regulating sphingosin-1 phosphate receptor 1 (S1Pr1). Here we show that this is not the case for B cells. Instead, KLF2 controls homeostasis of B cells in peripheral lymphatic organs and homing of plasma cells to the bone marrow, presumably by controlling the expression of β(7)-integrin. In mice with a B cell-specific deletion of KLF2, S1Pr1 expression on B cells was only slightly affected. Accordingly, all splenic B cell subsets including B1 cells were present, but their numbers were increased with a clear bias for marginal zone (MZ) B cells. In contrast, fewer peyers patches harboring fewer B cells were found, and fewer B1 cells in the peritoneal cavity as well as recirculating B cells in the bone marrow were detected. Upon thymus-dependent immunization, IgG titers were diminished, and antigen-specific plasma cells were absent in the bone marrow, although numbers of antigen-specific splenic plasmablasts were normal. KLF2 plays also a role in determining the identity of follicular B cells, as KLF2-deficient follicular B cells showed calcium responses similar to those of MZ B cells and failed to down-regulate MZ B cell signature genes, such as CD21 and CXCR7.     

Vertebrate-specific glutaredoxin is essential for brain development

Cellular functions and survival are dependent on a tightly controlled redox potential. Currently, an increasing amount of data supports the concept of local changes in the redox environment and specific redox signaling events controlling cell function. Specific protein thiol groups are the major targets of redox signaling and regulation. Thioredoxins and glutaredoxins catalyze reversible thiol-disulfide exchange reactions and are primary regulators of the protein thiol redox state. Here, we demonstrate that embryonic brain development depends on the enzymatic activity of glutaredoxin 2. Zebrafish with silenced expression of glutaredoxin 2 lost virtually all types of neurons by apoptotic cell death and the ability to develop an axonal scaffold. As demonstrated in zebrafish and in a human cellular model for neuronal differentiation, glutaredoxin 2 controls axonal outgrowth via thiol redox regulation of collapsin response mediator protein 2, a central component of the semaphorin pathway. This study provides an example of a specific thiol redox regulation essential for vertebrate embryonic development.