PMID- 37958975 OWN - NLM STAT- MEDLINE DCOM- 20231115 LR - 20231122 IS - 1422-0067 (Electronic) IS - 1422-0067 (Linking) VI - 24 IP - 21 DP - 2023 Nov 6 TI - Study on the Treatment of ITP Mice with IVIG Sourced from Distinct Sex-Special Plasma (DSP-IVIG). LID - 10.3390/ijms242115993 [doi] LID - 15993 AB - Intravenous immunoglobulin (IVIG) is a first-line drug prepared from human plasma for the treatment of autoimmune diseases (AIDs), especially immune thrombocytopenia (ITP). Significant differences exist in protein types and expression levels between male and female plasma, and the prevalence of autoimmune diseases varies between sexes. The present study seeks to explore potential variations in IVIG sourced from distinct sex-specific plasma (DSP-IVIG), including IVIG sourced from female plasma (F-IVIG), IVIG sourced from male plasma (M-IVIG), and IVIG sourced from a blend of male and female plasma (Mix-IVIG). To address this question, we used an ITP mouse model and a monocyte-macrophage inflammation model treated with DSP IVIG. The analysis of proteomics in mice suggested that the pathogenesis and treatment of ITP may involve FcgammaRs mediated phagocytosis, apoptosis, Th17, cytokines, chemokines, and more. Key indicators, including the mouse spleen index, CD16(+) macrophages, M1, M2, IL-6, IL-27, and IL-13, all indicated that the efficacy in improving ITP was highest for M-IVIG. Subsequent cell experiments revealed that M-IVIG exhibited a more potent ability to inhibit monocyte phagocytosis. It induced more necrotic M2 cells and fewer viable M2, resulting in weaker M2 phagocytosis. M-IVIG also demonstrated superiority in the downregulation of surface makers CD36, CD68, and CD16 on M1 macrophages, a weaker capacity to activate complement, and a stronger binding ability to FcgammaRs on the THP-1 surface. In summary, DSP-IVIG effectively mitigated inflammation in ITP mice and monocytes and macrophages. However, M-IVIG exhibited advantages in improving the spleen index, regulating the number and typing of M1 and M2 macrophages, and inhibiting macrophage-mediated inflammation compared to F-IVIG and Mix-IVIG. FAU - Zhang, Wei AU - Zhang W AD - Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China. FAU - Yuan, Xin AU - Yuan X AD - Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China. FAU - Wang, Zongkui AU - Wang Z AUID- ORCID: 0000-0002-5764-7660 AD - Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China. FAU - Xu, Jixuan AU - Xu J AD - Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China. FAU - Ye, Shengliang AU - Ye S AUID- ORCID: 0000-0003-4477-3075 AD - Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China. FAU - Jiang, Peng AU - Jiang P AD - Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China. FAU - Du, Xi AU - Du X AD - Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China. FAU - Liu, Fengjuan AU - Liu F AD - Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China. FAU - Lin, Fangzhao AU - Lin F AD - Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China. FAU - Zhang, Rong AU - Zhang R AUID- ORCID: 0000-0003-4480-7191 AD - Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China. FAU - Ma, Li AU - Ma L AD - Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China. FAU - Li, Changqing AU - Li C AD - Institute of Blood Transfusion, Chinese Academy of Medical Sciences & Peking Union Medical College, Chengdu 610052, China. LA - eng GR - 2023NSFSC0714, 2023ZHCG0066 and 2022YFS0010/Department of Science and Technology of Sichuan Province/ GR - CIFMS, 2021-I2M-1-042/CAMS Innovation Fund for Medical Sciences/ GR - Q22009/Scientific Research Project of Sichuan Medical Association/ PT - Journal Article DEP - 20231106 PL - Switzerland TA - Int J Mol Sci JT - International journal of molecular sciences JID - 101092791 RN - 0 (Immunoglobulins, Intravenous) RN - 0 (Cytokines) SB - IM MH - Male MH - Female MH - Humans MH - Animals MH - Mice MH - Immunoglobulins, Intravenous/therapeutic use MH - *Purpura, Thrombocytopenic, Idiopathic/drug therapy MH - *Thrombocytopenia/drug therapy MH - Cytokines MH - Inflammation/drug therapy PMC - PMC10648144 OTO - NOTNLM OT - IVIG sourced from distinct sex-specific plasma (DSP-IVIG) OT - immune thrombocytopenia OT - intravenous immunoglobulin OT - macrophages OT - proteomics COIS- The authors declare no conflict of interest. EDAT- 2023/11/14 06:43 MHDA- 2023/11/15 06:43 PMCR- 2023/11/06 CRDT- 2023/11/14 02:11 PHST- 2023/10/07 00:00 [received] PHST- 2023/10/30 00:00 [revised] PHST- 2023/11/03 00:00 [accepted] PHST- 2023/11/15 06:43 [medline] PHST- 2023/11/14 06:43 [pubmed] PHST- 2023/11/14 02:11 [entrez] PHST- 2023/11/06 00:00 [pmc-release] AID - ijms242115993 [pii] AID - ijms-24-15993 [pii] AID - 10.3390/ijms242115993 [doi] PST - epublish SO - Int J Mol Sci. 2023 Nov 6;24(21):15993. doi: 10.3390/ijms242115993.