The Intergroup Value Protection Model: A Theoretically Integrative and Dynamic Approach to Intergroup Conflict Escalation in Democratic Societies.

SCIENTIFIC ABSTRACT: We review social-psychological evidence for a theoretically integrative and dynamic model of intergroup conflict escalation within democratic societies. Viewing individuals as social regulators who protect their social embeddedness (e.g., in their group or in society), the intergroup value protection model (IVPM) integrates key insights and concepts from moral and group psychology (e.g., group identification, outrage, moralization, protest) into a functional intergroup value protection process. The model assumes that social regulators are continuously looking for information diagnostic of the outgroup's intentions to terminate the relationship with the ingroup, and that their specific cognitive interpretations of an outgroup's action (i.e., as a violation of ingroup or shared values) trigger this process. The visible value-protective responses of one group can trigger the other group's value-protective responses, thus dynamically increasing chances of conflict escalation. We discuss scientific implications of integrating moral and group psychology and practical challenges for managing intergroup conflict within democratic societies. PUBLIC ABSTRACT: The 2021 Capitol Hill attack exemplifies a major "trigger event" for different groups to protect their values within a democratic society. Which specific perceptions generate such a triggering event, which value-protective responses does it trigger, and do such responses escalate intergroup conflict? We offer the intergroup value protection model to analyze the moral and group psychology of intergroup conflict escalation in democratic societies. It predicts that when group members cognitively interpret another group's actions as violating ingroup or shared values, this triggers the intergroup value protection process (e.g., increased ingroup identification, outrage, moralization, social protest). When such value-protective responses are visible to the outgroup, this can in turn constitute a trigger event for them to protect their values, thus increasing chances of intergroup conflict escalation. We discuss scientific implications and practical challenges for managing intergroup value conflict in democratic societies, including fears of societal breakdown and scope for social change.

Human CD8(+) T cells and NK cells express and secrete S100B upon stimulation.

Previous studies have demonstrated the utility of S100B as a surrogate marker of brain-related pathologies, e.g. neuropsychiatric disorders, and melanoma progression, which have an inflammatory component. This study addresses the relevance of S100B(+) lymphocytes in mediating such responses. S100B expression was determined in human peripheral blood leukocytes isolated from healthy volunteers using flow cytometry. S100B(+) lymphocytes were characterised for phenotype, cytokine production and S100B secretion. In addition, we investigated whether S100B activates monocytes and neutrophils. S100B(+) cells comprised 2-4% of all lymphocytes and the majority displayed a CD3(+) CD8(+) phenotype; fewer cells were CD3(-) CD56(+) NK lymphocytes. Comparison of S100B(+) and S100B(-) CD3(+) CD8(+) cells revealed no differences in production of interferon gamma (IFNγ) and interleukin-2 (IL-2). Stimulation of S100B(+) CD3(+) CD8(+) lymphocytes with anti-CD3 or phytohaemagglutinin resulted in release of S100B. High concentrations of recombinant human S100B triggered upregulation of CD11b and membrane shedding of CD62L in granulocytes and monocytes. These findings set the stage for a new field of research addressing a S100B-mediated crosstalk between the innate and adaptive immune systems if close proximity of effector and responder cells accomplishes sufficient local S100B levels. In various physiological and pathological conditions S100B might function as an interface to immunological processes, distinct from known cytokine- and chemokine-mediated pathways.

Increased levels of serum IL-31 in chronic spontaneous urticaria.

IL-31 represents a novel cytokine involved in pruritic skin diseases including atopic dermatitis (AD). We, therefore, aimed at investigating IL-31 levels in chronic spontaneous urticaria (CU). We included 46 patients with CU, 26 non-atopic skin healthy subjects as negative and 28 patients with AD as positive controls. IL-31 serum levels were analysed using commercial ELISA kit. IL-31 serum levels were higher in patients with CU compared to healthy controls (P < 0.001), but lower compared to patients with AD (P < 0.001). There was no difference in IL-31 serum levels in autologous serum skin test positive or negative CU patients and patients with infectious trigger factors including helicobacter pylori infection. IL-31 serum levels may play a role in the pathophysiology of CU. This is supported by the finding that not all patients with CU respond to antihistamine treatment but to the treatment with immunosuppressive drugs.