The present research investigates whether benevolent and hostile sexist attitudes are differentially directed toward Black and White women by Black and White people. Participants (N = 2,775) reported on their sexist attitudes while thinking about Black women, White women, or women in general. Although Black participants reported higher levels of benevolent and hostile sexism overall, participant race and target race interacted to produce unique patterns of sexist attitudes. More specifically, Black perceivers thinking of White women reported higher levels of hostile sexism than those thinking of Black women. White perceivers reported similar amounts of hostile sexism while thinking of White and Black women. Benevolent sexism showed a different pattern, with both Black and White participants reporting higher levels of benevolent sexism toward Black than White women. The results also revealed similar levels of sexism reported while thinking of White women and while thinking of women in general, suggesting that sexism research that does not specifically address target race may reflect an understanding of sexist attitudes about White women that may not generalize to other racial groups.

Mycobacterium tuberculosis infection results in 1.5 million deaths annually. Type I interferon (IFN) signaling through its receptor IFNAR correlates with increased severity of disease, although how this increases susceptibility to M. tuberculosis remains uncertain. ISG15 is one of the most highly induced interferon stimulated genes (ISGs) during M. tuberculosis infection. ISG15 functions by conjugation to target proteins (ISGylation), by noncovalent association with intracellular proteins, and by release from the cell. Recent studies indicated that ISG15 can function via conjugation-independent mechanisms to suppress the type I IFN response. These data raised the question of whether ISG15 may have diverse and sometimes opposing functions during M. tuberculosis infection. To address this, we analyzed ISGylation during M. tuberculosis infection and show that ISGylated proteins accumulate following infection in an IFNAR-dependent manner. Type I IFN and ISG15 both play transient roles in promoting bacterial replication. However, as the disease progresses, ISGylation deviates from the overall effect of type I IFN and, ultimately, mice deficient in ISGylation are significantly more susceptible than IFNAR mice. Our data demonstrate that ISGs can both protect against and promote disease and are the first to report a role for ISGylation during M. tuberculosis infection.