Inflammatory bowel disease (IBD) includes ulcerative colitis (UC) and Crohn’s disease (CD), and its etiology and pathogenesis are still unclear. Most scholars believe that abnormal immune regulation, persistent intestinal infections, mucosal barrier defects, genetic and environmental factors are involved in the development of the disease. Patients with CD present with granulomatous inflammation of the entire mucosal tissue of the intestinal wall, mostly in the terminal ileum and ascending colon, but also in the oral, esophageal, gastric, and anal regions, with clinical manifestations such as abdominal pain, diarrhea, blood in the stool, and systemic manifestations such as weight loss, fever, and fatigue. The main manifestation is inflammation of the superficial mucosal tissue of the colonic wall, which may present with ulceration and acute purulent leukocyte infiltration. IBD is a complex disease caused by multiple factors, and both innate and acquired immune responses are involved in the development of the disease. Numerous studies have reported that the immunopathology of IBD is characterized by the specific activation of various lymphocytes in intestinal mucosal tissues by intestinal antigens.The inflamed intestinal mucosal tissues of IBD patients are infiltrated by a large number of activated immune cells, such as T cells, B cells, etc. Lymphocytes and some stromal cells (e.g. fibroblasts) within the intestinal mucosal tissue express high levels of adhesion molecules and helper signaling molecules. These immune cells also express high levels of cytokine receptors, chemokine receptors, integrins (e.g. a4b7 integrin), etc. in the inflammatory state, while capillary endothelial cells and fibroblasts within the intestinal mucosal tissue express high levels of chemokines, selectins, etc. on their surface. The interaction between these molecules further induces leukocytes in the blood circulation to move, homing and infiltrate into the intestinal mucosal tissues, contributing to the local inflammatory response. Abnormal immune response in intestinal mucosal tissues plays an important role in the development of intestinal inflammation in IBD patients. Isolation of CD4+ T cells in inflamed intestinal mucosal tissues of CD patients and in vitro stimulation revealed the production of a large number of Th1-effect pro-inflammatory cytokines, such as TNF-a, IL-2, IFN-g, etc. CD4+ T and NK-T cells in isolated inflamed intestinal mucosal tissues were found to secrete large amounts of Th2 cytokines such as IL-4, IL-5 and IL-13 after in vitro stimulation, whereas clinical immune features of UC patients mainly showed Th2-dominant immune response. These pro-inflammatory cytokines play a key role in the process of inflammatory damage in intestinal mucosa. The current clinical treatment for UC patients includes salicylates, glucocorticoids, antibiotics, probiotics, immunosuppressants, biologics, and surgical resection with the aims of inducing remission, maintaining remission, restoring and maintaining normal intestinal nutrition, maintaining the patient’s quality of life, and delaying and selecting the best time for surgery. In recent years, with the progress of research in molecular biology and immunology, there has been an in-depth understanding of intestinal immunopathology, especially the immunopathological mechanisms in UC patients, and new breakthroughs in bioimmunotherapy for UC. Many biologics have been used in animal models of colitis with promising results, and some biologics have shown good efficacy in clinical applications in IBD patients, bringing new light to targeted bioimmunotherapy for IBD patients. Biological therapies include monoclonal antibodies against pro-inflammatory cytokines, immune adhesion molecules, integrins, recombinant proteins, and antisense oligonucleotides. According to the mechanism of action, the main biological agents currently used in clinical practice are TNF-a monoclonal antibodies, inhibition of T-cell movement, inhibition of T-cell differentiation, inhibition of T-cell activation, promotion of intestinal epithelial cell repair, and local immunomodulation agents. 1.Block the biological activity of TNF-a: TNF-a is an important pro-inflammatory cytokine, which is considered as a mediator of the body’s resistance to tumors and infections, mainly secreted by T and Mf cells. TNF-a acts on two cell membrane receptors (i.e. TNFR1 or P55 subunit and TNFR2 or P75 subunit) to exert biological effects. TNFR1 can bind soluble TNF-a, while TNFR2 mainly binds to model TNF-a to exert signaling effects, leading to cell death, inflammation development and fibrous tissue proliferation. The first antibodies used in clinical practice to block the biological activity of TNF-a are anti-TNF-a monoclonal antibodies and TNF receptor fusion proteins, etc. The first anti-TNF-a monoclonal antibody used in clinical practice, Infliximab, is a chimera of mouse IgG1 and anti-human TNF-a monoclonal antibody. This chimeric antibody has low immunogenicity, high blood concentrations, and rapid onset of action, usually within 2 weeks, with approximately 50% of UC patients achieving clinical remission and drug effects lasting several weeks to six months. Infliximab is recommended for the treatment of active CD patients with fistula formation at 5 mg/kg intravenously (0, 2, and 6 weeks) and has shown good efficacy in promoting fistula healing, reducing peripheral blood C-reactive protein (CRP) and IL-6 levels, preventing relapse with maintenance therapy (1 dose/8 weeks), and being well tolerated by patients with a low incidence of side effects. In clinical studies, Infliximab has been found to provide rapid remission, but the long-term remission rate alone is not significant, mainly due to the high recurrence rate and the need for surgery in 1/3 of patients. In recent years, a number of side effects related to immunity and infection have been found with long-term use of Infliximab. Anti-Infliximab antibodies (ATI) are induced in CD patients treated with Infliximab, with ATI occurring in 30%-61% of patients treated in acute exacerbations and only 8%-16% in remission maintenance therapy. 2-fold more intravenous infusion reactions occur in ATI-positive patients than in ATI-negative patients (16%-30% vs. 8%-16 %). Some reports have also demonstrated a 12% increase in IV response with the presence of ATI antibodies. Common side effects during the use of Infliximab include headache, dizziness, nausea, skin irritation at the injection site, flushing, chest pain, dyspnea, and pruritus. In addition, Infliximab can also cause anti-double-stranded helix DNA antibodies (dsDNA, 23.3%-34%), anti-nuclear antibodies (ANA, 46%-56%), drug-induced systemic reactions (0.2%), upper respiratory and urinary tract infections (30%-34%), and opportunistic infections (Nocardia, cytomegalovirus, histoplasmosis, invasive pulmonary aspergillosis). pulmonary aspergillosis), acute tuberculosis infection, lymphoma, optic neuritis, multiple motor neuron disease, and drug-induced lupus. Inhibit the movement of lymphocytes to the inflammation site: Surface adhesion molecule (ADM) has the function of regulating the movement of leukocytes in the intestinal mucosal tissue vasculature to the intertissue, and is involved in the antigen presentation and lymphocyte activation in the intestinal mucosa. Alicaforsen (ISIS 2302) is an antisense oligonucleotide of ICAM-1. Natalizumab and MLN-02 are the antisense oligonucleotide of ICAM-1. a4b7 integrin human IgG4 monoclonal antibody that selectively blocks signaling between a4b7 and MAdCAM-1, a4b1 and VCAM-1, and inhibits the movement of leukocytes to sites of inflammation. Experimental phase III clinical treatment has been performed, administered intravenously (3 mg/kg) at weeks 0, 4 and 8, showing significant relief of disease activity in UC patients, with common side effects such as headache, abdominal pain, vomiting and sore throat. In clinical studies, Natalizumab was found to be effective in relieving the symptoms of patients with active UC, with significant improvement in intestinal mucosal histology. 3 mg/kg IV alone for 2, 4, and 8 weeks was found to be 20%, 30%, and 80% effective, respectively, and to reduce blood C-reactive protein levels, with side effects such as allergic reactions at the injection site, headache, fever, and arthralgia. recombinant of a4b7 integrin monoclonal antibody and human IgG1, selectively blocks the signaling between a4b7 and MAdCAM-1 and inhibits the movement of leukocytes to the site of inflammation. It has been clinically treated in UC patients in phase I/II trials with some clinical efficacy. 3, inhibition of T-cell activation: The main anti-CD3 monoclonal antibody. It was found that there is a large infiltration of activated T cells in the inflammatory intestinal mucosal tissue of UC patients. T cells in the inflammatory intestinal mucosal tissue were isolated and analyzed to express high levels of activation markers, and in vitro culture revealed that T cells secrete high levels of pro-inflammatory cytokines (such as IL-4, IL-13, TNF-a, etc.). visilizumab is an anti-human CD3 monoclonal antibody that acts directly on the T cell surface CD3 molecules and inhibits the effector response of T cells. The application in UC patients showed significant relief of clinical symptoms and contributed to the repair of colonic mucosal ulcers, but some patients showed side effects such as nausea, fever and arthralgia. Basiliximab is a chimeric anti-CD25 monoclonal antibody that blocks the binding of IL-2 to IL2R and inhibits T cell appreciation. Treatment of patients with moderate-to-severe UC with the Daclizumab antibody resulted in no significant improvement in clinical remission rates in UC patients over placebo, but was well tolerated by patients with few side effects. In other clinical trials, Basiliximab antibody was found to be used to treat hormone-resistant moderate-severe UC (general dosage 40 mg, i.v.), with the addition of prednisone tablets (30 mg/day) for patients with moderate UC and hydrocortisone injections (400 mg/day, i.v. drip) for patients with severe UC until after stool frequency less than 3 times/day or no visible blood in the flesh After Basiliximab was administered, the clinical remission rate reached 50% within 8 weeks and 65% at 24 weeks, with few side effects and safe clinical use. 5.Therapeutic leukocytapheresis: The use of non-nylon polyester membrane to selectively remove activated neutrophils and monocytes from peripheral blood through extracorporeal blood circulation has a significant effect on the clinical symptoms of active, hormone-dependent patients with moderate-to-severe UC and active CD patients, and can upregulate serum IL-1 receptor antagonist (IL-1Ra) and IL-1Ra. (IL-1Ra) and IL-10 levels with low side effects. Currently, the clinical treatment of IBD patients mostly adopts a step-up drug treatment strategy, i.e., 5-ASA agents, glucocorticoids → immunosuppressive agents → bioimmune agents. However, in recent years, with the clinical application of biological agents such as infliximab, it has been found that it can effectively relieve the disease and promote the repair of intestinal mucosal inflammation, so some people advocate the use of step-down treatment strategy, i.e., first use of biological immune agents and/or combined immunosuppressive agents to achieve rapid remission and reduce the emergence of complications, and then use 5-ASA maintenance therapy. The clinical use of biologic immune agents has brought about a significant improvement in IB. The clinical application of bioimmune agents has brought new light to the treatment of IBD patients and added new therapeutic measures to the majority of clinicians. Currently, laboratory studies have reported that many biological agents (e.g., monoclonal antibodies, fusion proteins, synthetic peptides, etc.) have shown good efficacy in animal models of experimental colitis, prompting intestinal inflammatory repair and inhibiting the secretion of pro-inflammatory cytokines by lymphocytes in intestinal mucosal tissues, but only a small number of biological agents have shown some efficacy in patients with IBD, and the long-term clinical efficacy, occurrence of side effects, and effects on The long-term clinical efficacy, the occurrence of side effects, and the effect on the genetic inheritance of patients need to be further verified. These clinical data need to be further studied and observed with long-term follow up. It should be done by laboratory researchers, bioengineering experts, and clinicians in order to obtain reliable theoretical data to guide clinical workers in the clinical treatment of patients. Therefore, when formulating a treatment plan for patients with IBD (especially when selecting biologics), comprehensive consideration and careful deliberation are needed in conjunction with the patient’s condition to rationally select drugs.