Racism behind the screen: Examining the mediating and moderating relationships between anonymity, online disinhibition, and cyber-racism.

Cyber-racism has emerged as a societal issue that affects many youths and adults; however, no published work has elucidated the psychological processes germane to predicting cyber-racism perpetration. Theory-without data to support its postulates-argues that online disinhibition mediates the relationship between anonymity afforded the online user and cyber-racism. The purpose of the current research was to examine this prediction and add to the theory by testing additional mediators and moderators. Six empirical studies tested this theory with U.S. adults, and results reliably showed that online disinhibition mediated the relationship between anonymity and cyber-racism. Moreover, we also found evidence to suggest that (a) this mediated effect remained while controlling for real-world variables, (b) the mediated effect was moderated by racial prejudice, (c) the mediated effect was moderated by cyberbullying perpetration, and (d) that certain types of online disinhibition are stronger mediators than others. Finally, Study 7 synthesized these six studies and found evidence for the mediating influence of online disinhibition in the relationship between anonymity and cyber-racism. (PsycInfo Database Record (c) 2023 APA, all rights reserved).

Understanding Cyber-Racism Perpetration within the Broader Context of Cyberbullying Theory: A Theoretical Integration.

The purpose of the current theoretical review is to argue for the theoretical integration of cyber-racism perpetration into the broader cyberbullying context-making note of the similarities between both types of nefarious online behavior that make this integration appropriate and the differences that make the integration less clear. Cyber-racism and cyberbullying victimization have been shown to be prevalent in youth and is related to poor psychological outcomes. Understanding both types of antisocial online behaviors have implications for the understanding and subsequent reduction of cyber-racism. Our review focuses on a cyber-racism model that proposes the importance of anonymity perceptions afforded to the online user to cause cyber-racism via several routes that focus on (a) online disinhibition, (b) deindividuation and group polarization, and (c) stereotypes. We discuss the tenets of this theory and the overlap with the Barlett Gentile Cyberbullying Model-a learning-based model that focuses on how anonymity eventually predicts cyberbullying via the development of positive cyberbullying attitudes. We believe that theoretical integration is necessary; however, future work needs to test several theoretical underpinnings of these models first. We end with a discussion of theoretical and intervention implications before discussing limitations and future work. Overall, we hope this review sparks interesting future research to understand cyber-racism and broaden the existing research on cyberbullying.

Epicutaneous challenge of orally immunized mice redirects antigen-specific gut-homing T cells to the skin.

Patients with atopic dermatitis (AD) often suffer from food allergy and develop flares upon skin contact with food allergens. However, it is unclear whether T cells sensitized to allergens in the gut promote this skin inflammation. To address this question, we orally immunized WT mice and mice lacking the skin-homing chemokine receptor Ccr4 (Ccr4-/- mice) with OVA and then challenged them epicutaneously with antigen. Allergic skin inflammation developed in the WT mice but not in the mutants and was characterized by epidermal thickening, dermal infiltration by eosinophils and CD4+ T cells, and upregulation of Th2 cytokines. T cells purified from mesenteric lymph nodes (MLNs) of orally immunized WT mice transferred allergic skin inflammation to naive recipients cutaneously challenged with antigen, but this effect was lost in T cells purified from Ccr4-/- mice. In addition, the ability of adoptively transferred OVA-activated T cells to home to the skin following cutaneous OVA challenge was ablated in mice that lacked lymph nodes. These results indicate that cutaneous exposure to food antigens can reprogram gut-homing effector T cells in LNs to express skin-homing receptors, eliciting skin lesions upon food allergen contact in orally sensitized AD patients.

Characterizing the relationship between sesame, coconut, and nut allergy in children.

Sesame and coconut are emerging food allergens in the United States. We sought to examine whether children allergic to peanuts and tree nuts are at increased risk of having an allergy to sesame or coconut. We performed a retrospective chart review of children who underwent skin prick testing (SPT) to sesame and coconut and identified 191 children who underwent SPT to sesame and 40 to coconut. Sensitization to sesame was more likely in children with positive SPT to peanuts (odds ratio [OR] = 6.7, 95% confidence interval [CI] [2.7-16.8], p < 0.001) and tree nuts (OR = 10.5, 95% CI [4.0-27.7], p < 0.001). Children with histories of both peanut and tree nut reaction were more likely to have a history of sesame reaction (OR = 10.2, 95% CI [2.7-38.7], p < 0.001). Children with sensitization or allergy to peanuts or tree nuts were not more likely to be sensitized or allergic to coconut. In conclusion, children with peanut or tree nut sensitization were more likely to be sensitized to sesame but not coconut. Children with clinical histories of both peanut and tree nut allergy were more likely to be allergic to sesame.

Sesame allergy: role of specific IgE and skin-prick testing in predicting food challenge results.

There are conflicting data regarding the diagnostic value of sesame-specific IgE and sesame skin test. Currently, there are no established thresholds that predict clinical reactivity. We examined the correlation of sesame ImmunoCAP and skin-prick test (SPT) results with oral challenge outcomes in children suspected of having a sesame food allergy. We conducted a retrospective chart review of children, aged 2-12 years, receiving a sesame ImmunoCAP level, SPT, and food challenge from January 2004 to August 2008 at Children's Hospital Boston and affiliated allergy clinics. Food challenges were conducted in cases of questionable clinical history or a negative ImmunoCAP and/or negative SPT despite a convincing history. Thirty-three oral sesame challenges were conducted. Of the 33 challenges performed, 21% (n = 7) failed and 79% (n = 26) passed. A sesame-specific IgE level of > or = 7 kU(A)/L showed specificity of >90%. An SPT wheal size of > or = 6 mm showed specificity of >90%. Receiver operator characteristic (ROC) curve analysis for sesame-specific IgE revealed an area under the curve (AUC) of 0.56. ROC curve analysis for SPT wheal size revealed an AUC of 0.67. To our knowledge, this study represents the largest number of sesame challenges performed to evaluate the diagnostic value of both sesame-specific IgE and SPT. Based on our sample, both tests are not good predictors of true sesame allergy as determined by an oral challenge. We were unable to establish a threshold with a 95% positive predictive value for both sesame-specific IgE and SPT.

Vaccinia virus inoculation in sites of allergic skin inflammation elicits a vigorous cutaneous IL-17 response.

Eczema vaccinatum (EV) is a complication of smallpox vaccination occurring in patients with atopic dermatitis. In affected individuals, vaccinia virus (VV) spreads through the skin, resulting in large primary lesions and satellite lesions, and infects internal organs. BALB/c mice inoculated with VV at sites of Th2-biased allergic skin inflammation elicited by epicutaneous ovalbumin (OVA) sensitization exhibited larger primary lesions that were erosive, more satellite lesions, and higher viral loads in skin and internal organs than mice inoculated in saline-exposed skin, unsensitized skin, or skin sites with Th1-dominant inflammation. VV inoculation in OVA-sensitized skin induced marked local expression of IL-17 transcripts and massive neutrophil infiltration compared to VV inoculation in saline-exposed skin. Treatment with anti-IL-17 decreased the size of primary lesions, numbers of satellite lesions, and viral loads. Addition of IL-17 promoted VV replication in skin explants. These results suggest that IL-17 may be a potential therapeutic target in EV.

Impaired immune response to vaccinia virus inoculated at the site of cutaneous allergic inflammation.

BACKGROUND: Patients with atopic dermatitis (AD) exposed to the vaccinia virus (VV) smallpox vaccine have an increased risk of developing eczema vaccinatum. OBJECTIVE: To investigate the effects of local allergic skin inflammation on vaccinia immunity. METHODS: BALB/c mice were epicutaneously sensitized with ovalbumin (OVA) to induce allergic skin inflammation or with saline control, then inoculated with an attenuated VV strain by skin scarification or intraperitoneally. After 8 days, serum IgG anti-VV and cytokine secretion by splenocytes were measured. RESULTS: Mice inoculated with VV at sites of epicutaneous sensitization with OVA, but not control mice inoculated at saline exposed sites, developed satellite pox lesions and had impaired secretion of T(H)1 cytokines in response to VV, decreased VV specific serum IgG(2a), increased VV specific serum IgG(1), and impaired upregulation of IFN-alpha, but not the cathelicidin-related antimicrobial peptide, at the infection site. The VV immune response of OVA-sensitized mice inoculated with VV at distant skin sites or intraperitoneally was normal. CONCLUSION: Local immune dysregulation at sites of allergic skin inflammation underlies the impaired T(H)1 immune response to VV introduced at these sites and the increased susceptibility to develop satellite pox lesions, a characteristic of eczema vaccinatum in patients with AD. CLINICAL IMPLICATIONS: In a mouse model of AD, inoculation of VV at inflamed skin sites is associated with increased numbers of satellite pox lesions and an abnormal immune response to the virus. This may contribute to the susceptibility of patients with AD to virus dissemination after smallpox vaccination.