The present invention relates to methods for modulating immune response based on binding I-domain of CD11b on the tumor associated myeloid cells (TAMCs) in the tumor microenvironment. Particularly, binding to I-domain of CD11b with anti-CD11b-I-domain antibody triggers immunostimulatory environment that have one or more of the following effects in the tumor microenvironment: increase the inflammatory cytokine in the tumor microenvironment, decrease the population of IDO+ myeloid suppresser cells, up-regulate M1 marker over M2 marker on the tumor associated macrophage, increase M1:M2 tumor associated macrophage ratio, promote differentiation of dendritic cells (DC), nature killer dendritic cells (NKDC), and plasmacytoid dendritic cells (pDC), increase population of 4-1BB+PD-1+ neoantigen specific CD8 T cells. Converting cold (non-inflamed) to hot (inflamed) tumor by binding to I-domain of CD11b with anti-CD11b-I-domain antibody allows enhanced effectiveness of immune response modulator.本發明係關於基於在腫瘤微環境中結合腫瘤相關骨髓細胞(TAMC)上之CD11b之I域，來調節免疫反應之方法。特定言之，使用抗CD11b-I域抗體結合至CD11b之I域，以觸發免疫刺激環境，其在該腫瘤微環境中具有以下一或多種效果：增加該腫瘤微環境中之發炎性細胞介素、減少IDO+骨髓抑制細胞之數目、在腫瘤相關巨噬細胞上相較於M2標記物上調M1標記物、增大M1:M2腫瘤相關巨噬細胞比率、促進樹突狀細胞(DC)、自然殺手樹突狀細胞(NKDC)及漿細胞樣樹突狀細胞(pDC)分化、增加4-1BB+PD-1+新抗原特異性CD8 T細胞之數目。藉由用抗CD11b-I域抗體結合至CD11b之I域將冷的(未發炎的)腫瘤轉化為熱的(發炎的)腫瘤，以增強免疫反應調節劑之有效性。
