Psoriasis is a chronic inflammatory condition influenced by genetic, environmental, and immunological factors. Emerging studies have highlighted the significant influence of the microbiome in the pathogenesis of psoriasis. Lactobacillus reuteri, a probiotic bacterium commonly found in the gastrointestinal tract, has garnered significant attention due to its anti-inflammatory properties and its ability to modulate the host immune system, which could be beneficial in managing psoriasis. In this study, we investigated the therapeutic effect of heat-killed L. reuteri on imiquimod induced psoriatic-like mice. The findings indicated that heat-killed L. reuteri (NCHBL-005) led to a reduction in the Psoriasis Area Severity Index (PASI) and proinflammatory cytokines. Additionally, NCHBL-005 reduced significantly dorsal skin thickness in the NCHBL-005 treated group compared to the Imiquimod-induced psoriasis mouse group. The analysis of Th17 cells expressing IL-17A showed a decrease in topical application of NCHBL-005 group. The mechanism of NCHBL-005 in imiquimod-induced psoriasis was investigated in relation to NOD2, TLR2, and the Aryl Hydrocarbon Receptor (AhR). The psoriasis-alleviating effects of NCHBL-005 were observed in NOD2 ^-/- and TLR2 ^-/- mice. Conversely, the absence of psoriasis-relieving effects of NCHBL-005 in AhR⁺^/⁻ mice suggests that its therapeutic action is mediated via the AhR pathway. Altogether, our data demonstrate NCHBL-005 alleviates psoriasis symptoms, indicating its potential role in psoriasis treatment.