Abstract: Intergroup Empathy Bias refers to the phenomenon characterized by differential empathic responsiveness toward in-group versus out-group members. The neurobiological substrates of this bias - particularly its associated functional neurocircuitry and neuroregulatory processes - remain incompletely characterized. To systematically identify consistent neuroanatomical regions implicated in intergroup empathy bias and elucidate their neurofunctional correlates, this investigation implements a tripartite methodological framework:
Phase I utilizes Activation Likelihood Estimation (ALE) to systematically map convergent neuroanatomical patterns associated with intergroup empathy bias. Stratified subgroup analyses are implemented to investigate moderating variables: affective dimensions (nociceptive vs. emotional processing), social categorization paradigm (racial vs. non-racial grouping), and task design characteristics (implicit vs. explicit empathy paradigms). Phase II applies Meta-Analytic Connectivity Modeling (MACM) to delineate functional connectivity between identified neural hubs and distributed cortical networks. The final phase leverages Neurosynth - a comprehensive neuroimaging meta-analysis platform integrating data from over 14,000 task-based fMRI studies - to characterize functional profiles of the identified network during intergroup empathy processing.
This study employs ALE meta-analysis to analyze neuroimaging coordinates from 19 independent experiments on intergroup empathy bias. Two suprathreshold activation clusters exhibit robust convergence: the left anterior insula (lAI) and medial prefrontal cortex (mPFC). This lateralization reflects differential functional specialization: left insular activity is modulated by social group categorization during affective processing, whereas right insular functions (e.g., attentional modulation, network reconfiguration) are categorization-insensitive. Critically, in-group conditions demonstrating mPFC activation magnitude proportional to negative affect intensity highlight this region's regulatory dominance. Post hoc subgroup analyses reveal task-dependent neural signatures: affective rating paradigms predominantly recruit the lAI through heightened subjective emotional resonance mechanisms, whereas emotion categorization tasks engage mPFC-mediated executive control circuitry via deliberate cognitive appraisal processes.
Through MACM and Neurosynth functional decoding, this study reveals robust functional interconnectivity between the two neural clusters and distributed cortical/subcortical regions, indicating an evolutionarily optimized network architecture for intergroup empathy modulation. The network's operational mechanisms are conceptualized through three neurocognitive dimensions: (1) Executive regulation - mirroring Central Executive Network (CEN) dynamics via prefrontally mediated cognitive control; (2) Affective modulation - suppressing out-group empathy through dual pathways: impaired emotion recognition (ventral anterior cingulate cortex [vACC] hypoactivation) and diminished emotional resonance (reduced mirror neuron system efficacy); (3) Motivational valuation - striatal-orbitofrontal circuits perform neuroeconomic cost-benefit analyses, wherein in-group empathy demonstrates heightened utility in social exchange frameworks.
By synthesizing neuroimaging meta-analytic evidence, this study delineates consistent neural substrates underlying intergroup empathy bias, thereby proposing a theoretical framework to guide subsequent research. Furthermore, these empirical insights provide a neural foundation for precision-targeted neuromodulatory interventions. Systematic identification of critical neuroanatomical regions and their networks enables the development of optimized neuroregulatory strategies. These strategies aim to ameliorate intergroup empathy bias, ultimately fostering societal cohesion and enhancing cooperative dynamics.

Key words: intergroup empathy bias, ALE meta-analysis, MACM, Neurosynth