In the United States, roughly one out of every eight couples, or 7.5 million women, experience challenges related to conceiving or maintaining a pregnancy. The body's immune response is vital during pregnancy. T cells, natural killer (NK) cells, B cells, and macrophages (MQ) are immune cells in the female reproductive tract. They are in charge of maintaining tissue homeostasis and regulating the immune system's response to invasive pathogens. Failure to regulate these immune cells might result in inflammation, which reduces fertility. The immune system modulation of pregnancy loss has been studied with intralipid, intravenous immunoglobulin (IVIG), and paternal leukocyte vaccination. A concentrated antibody called intravenous immunoglobulin (IVIG) is utilized as a biological agent to treat autoimmune, viral, and inflammatory diseases and some immunodeficiencies. The main objective of this treatment is to restore a damaged immune system. IgGs, through binding to specific antigens, promote the innate immunity's cellular and humoral immune response by activating complements and binding to Fc receptors of several immune cells. Contrariwise, IVIG regulates pathogenic autoimmunity in animal models, including skin-blister diseases, nephrotoxic nephritis, and K/BxN arthritis. IVIG has, therefore, been of great interest as an immune modulator in several immune disorders. This review aims to investigate the immunological reasons of reproductive failure, focusing on the immunomodulatory effects of IVIG in its treatment.