MindMap Gallery Medical Immunology—Transplantation Immunity Mind Map
This is a mind map about medical immunology-transplantation immunity, including transplantation antigens/histocompatibility antigens, clinical types, prevention and treatment principles, etc.
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This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
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transplant immunity
Transplantation Antigen/Histocompatibility Antigen
Major Histocompatibility Antigen (MHC)
Minor histocompatibility antigen (mH)
Human ABO blood group antigen
tissue specific antigen
mechanism
T cells play central role in transplant rejection
mechanism
Recognition of alloantigens by T cells
direct identification
Donor APC carries p-MHC→recipient T cells
Fast, strong, plays a major role in acute rejection reactions
There are 1 to 10% of T cells in the human body that can recognize allogeneic MHC
indirect identification
Recipient APC uptakes and processes graft MHC antigen → recipient T cells
Plays an important role in acute rejection, late stage and chronic rejection
T cell activation and efficacy
Produce chemokines and form cell infiltration dominated by mononuclear cells
CD8 CTL
CD4 TH1, TH17
Humoral immunity
Mainly IgM
clinical type
Host versus graft reaction (HVGR)
Hyperacute rejection reaction—within 24 hours
reason
The pre-existing antibodies in the recipient's body bind to the antigen, activating the complement and coagulation systems, leading to vascular coagulation.
Pre-stored antibodies come from
ABO/RH blood type incompatibility between donor and recipient
The recipient has repeated blood transfusions, is pregnant, or has had some type of transplant in the past
Acute rejection—a few days to two weeks
Cellular immunity—acute interstitial inflammation
Cytotoxicity of CD8 Tc
CD4 Th-mediated delayed-type hypersensitivity
other cells
Humoral immunity—acute vasculitis
Activating complement (same as hyperacute rejection)
Chronic rejection—months to years
Immunological mechanism
Cytotoxicity of specific antibodies or effector cells on microvascular endothelial cells, leading to vascular damage
Chronic delayed-type hypersensitivity induces macrophages to secrete smooth muscle cell growth factors, leading to smooth muscle hyperplasia, arteriosclerosis, etc.
non-immunological mechanisms
Degenerative changes in tissues and organs
Graft versus host reaction (GVHR)
condition
MHC mismatch between host and graft
The graft contains a sufficient number of immune cells
The host is in a state of immune incompetence or severely deficient immune function
clinical scope
Most – bone marrow transplant
Rarely – thymus, small intestine and liver transplants
type
Acute graft-versus-host reaction (aGVHR)
Occurs within days to 2 months after transplantation
Manifested by apoptosis, death and inflammatory cell infiltration
Causes cell necrosis in multiple organs such as skin, liver and intestines
Mainly Th1 and Th17 mediated inflammatory response and CTL cytotoxic effect
NK, DC, and macrophages are also involved
Chronic graft-versus-host reaction (cGVHR)
After 100 days, 20-70% of patients develop cGVHR
Fibroproliferative changes, mechanism unknown
Prevention and control principles
Donor screening
ABO/RH blood group antigen matching
HLA gene matching
Mainly with DR, A and B (type II antigens are more important than type I antigens)
HLAI class gene matching (A, B, C)
HLA II gene matching (DP, DQ, DR)
crossmatch
Donor serum + recipient leukocytes were mixed for immunofluorescence test
Rule out the possibility of pre-produced anti-donor antibodies in the recipient
Graft and Recipient Preconditioning
Graft conditioning
Remove remaining white blood cells—DC, macrophages, T cells—from the graft
Recipient pretreatment
Plasma exchange, immunosuppressive therapy
Monitoring of rejection after transplantation
Detection of humoral immunity—blood group antibodies, HLA antibodies, donor antigen antibodies
Detection of cellular immunity—related cell numbers, functions, and cytokine levels
Detection of complement levels—complement content and activity
Application of immunosuppressants
Chemical immunosuppressants—glucocorticoids, cyclosporine A, etc.
Chinese herbal immunosuppressants
induction of immune tolerance
costimulatory molecule
Blockade of positive costimulatory signals
CD40-CD40L, B7-CD28, etc.
Enhancement of negative costimulation signals
PD-1, CTLA4, etc.
Adoptive transfer of regulatory cells: tolerant DC, Treg, MDSC, etc.
Splenectomy, radiation irradiation graft, etc.