basic immunology and transplantation · basic immunology and organ transplantation ahmed...
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BASIC IMMUNOLOGY and
ORGAN
TRANSPLANTATION
Ahmed Mahmoud,MD
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Host defense against infection
is 1-nonspecific or
2-specific (immune system)
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NONSPECIFIC
• Starts in the blood by
– 1) leucocytes phagocytosis and
– 2)activation of the complement system
both classic and alternative
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• Phagocytosis occurs mainly by leucocytes,
which is considered to be the most
important cell for phagocytosis .
• It also occurs by macrophages, but
leucocytes are more efficient and more in
number.
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• In tissues ,macrophages engulf and
phagocytose the bacteria.
• The secretion of monokines and other
mediators of inflammation (platelet
activating factor and leucotrines),
complement activation (classic by IgM and
IgG) or alternative by endotoxin of Gm-ve
…
• All these will lead to recruitment of PMNL
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• PMNL appear early and the bone marrow
responds to IL3 (colony stimulating factor)
by releasing more PMNL.
• Half life time is 12 hours in the circulation
and 24 hours in the tissues . Because of
quickness of release of PMNL from the
bone marrow, some are still premature and
have some bands .
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Two types of Phagocytes can be
differentiated
• 1-circulating=granulocytes and monocytes
• 2-fixed = macrophages
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PMNL have 3 functions
• 1)chemotaxis= migration by many chemotactic
factors
the most important is C5A
• 2) Phagocytosis= occurs by adherence then
opsonisation .
the most potent opsonins are C3B
IgM is the best immunoglobulin to fix complement
• 3) intracellular killing
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• PMNL have receptors for IgGs, C3B, ..
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SPECIFIC FUNCTION
• HUMORAL (B CELL)
• CELLULAR (T CELL)
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AFFERENT
CENTER
EFFERENT
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AFFERENT
CENTER
EFFERENT
Antigen presenting
cellCD4 -CD8
-B Lymphocytes
-NK
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Humoral
B Lymphocytes• B lymphocytes will originate and grow in
the Bone marrow. IL7 for early development
• They produce Immunoglobulins in response to antigens .
• The B cells when activated are called Plasma cells (have more condensed Golgi apparatus).
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• The immunoglobulins ( IgG, IgM ….)
released by the B cells act as receptors for
the B cells and link them to the Antigen .
• The Antigen then becomes opsonised by
the B cells.
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• The Antibody bound surfaces also activates a destructive enzymatic cascade known as the Complement system.
• The activation of the Complement causes multiple effects e.g
opsonisation ,chemotaxis, membrane attack complex, Stimulation of factor XI of coagulation, fibrinolysis , Kallikerin ..
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• B cells (unlike T cells) do not need MHCto recognize antigen .
• Immunoglobulins (IgG ,IgM….) act like receptors for B cells , just like T cell receptors for T cells
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• IgM is the first to appear but later changes
to other more specific IgG or IgM ..
• IgA is the mucosal immune antibody
• IgE for mast cell mediated immunity
• The cytokines responsible for B cells
activation are IL2 , IL 4,IL6 and IL7 for
early maturation
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• Hyperacute rejection is related to preformed
natural antibody on Donor endothelium
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Cell Mediated Immunity
T lymphocytes
• T lymphocytes originates in the bone marrow but mature in the Thymus.
• Acquire a specific receptor T cell receptor =TCR.
• T cells can not recognize antigens without aTCR . The antigen has also to be associated with MHC II (HLA II) to be recognized by the T cell receptor
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• The TCR is antigen specific and has alpha, beta subdimer and an essential part is CD3
• All TCR have CD3
• The TCR also has either
• CD4 or CD8
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• Resting (non activated)T cells do not express IL2
receptors .
• Only when stimulated by a specific antigen with
MHC II at the T cell receptor, they then express IL2
receptors and bind the IL2 to become active in
inducing more Tcells to express IL2 receptors .
• This is why IL2 inhibitors e.g Cyclosporin(mainly
used in kidney) and (Tacrolimus=Prograf
=FK506)(mainly used in liver) FK506 are
important.
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• T helper cells (Th1 ,Th2) have CD4
• T cytotoxic cells(Tc1,Tc2) have CD8
For CD8 to act on targets, an MHC I has to
be present
• Interferon Gamma increases the
expression of MHC I (HLA I) on the cells to
be attacked.
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Immune Response(Afferent &efferent)
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• Antigen presenting cells
• Are B Cells, macrophages and dendritic
cells , langherans cells
They ingest antigens, process them ,then
express them on their surface for TCR ., in
association with MHC II (HLA II)
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• Major Histocompatibility Complex (HLA)
– transmembrane glycoproteins which are encoded by the short arm of chromosome 6
– have a high degree of sequence polymorphism
– Type I; A,B,C .
– Present on all nucleated cells ,including T cells,B cells and platelets and are targets for cytotoxic CD 8 T cells = efferent limb of the immune response
– Type II; DR ,DP ,DQ
– present only on B lymphocytes, monocytes, macrophages and some activated T cells but not onunstimulated T cells. It is the afferent limb of the immune response
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Why HLA matching is NOT
commonly followed• HLA matching test takes time . Remember that organ ischemia
time (graft is not perfused ) is more important than HLA matching for the graft to survive and function in the recipient . No preservation solution is ideal
• Early long term graft survival is equal in HLA matched or mismatched,
long term (> 5 years) graft survival , however, is better in matched transplants
Necessity of transplantation is more pressing e.g end stage liver disease
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• HLA cross matching is highly
recommended for living related kid Tx . It
may also be done for Cadaveric kid since it
may increase the long term graft survival .
• > 5 mismatching is a relative
contraindication
• DR ,DQ are the more important
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Graft survival ; HLA matched
/mismatched
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Complications of Transplantation
• Hyperacute rejection; 1% . preformed
antibodies. Occurs immediately after release of
clamp and is irreversible.
No treatment available.
• Should be prevented by conducting the Final
Lymphcytotoxic cross match to detect IgG
antibodies directed against class I MHC
• Positive Cross match is a contraindication
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Cross match ; panel /final
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• Acute rejectionT cell mediated , treated with steroids initially with 90 % success rate .
• Occurs any time after day 5 of Transplantation as unexplained function deterioration .
• Organ is infiltrated with T cells.(diagnostic)
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• Chronic rejection seen after 1 or 2 years as
gradual deterioration of function
• Chronic rejection is called;
• Broncholitis obliterans in lung
• Vanishing Bile duct syndrome in Liver
• Endarteritis obliterans in heart
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Complication of transplantation
• Infection
• First month= usual post op infection
• 2 to 6 month = opportunistic infection e.g CMV – Pneumocystis-Aspergillosis
• After 6 months = low incidence of infection
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• Malignancy
• Skin tumors SCC > BCC (cardiac transplant)
• B cell Lymphoma (EB virus infection)=
• Post Transplant Lymphoproliferative Disorders =
PTLD - discontinue IL II inhibitors
• give Gancyclovair for EB virus infection
• Cardiovascular disease
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Question
• The most common cause of mortality within
the first year after renal Tx is
• A.Malignant tumors
• B.Cardiovascular disease
• C.Sepsis
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Early and late mortality after
Renal TX
• EARLY ( 1 st YEAR)
• Sepsis 45%
• CVS 35%
• LATE (2-17 YEARS)
• CVS 35 %
• Malignancy 20%
• Sepsis 19%
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Brain dead Donor
• Avoid hypotension and hypoxia
• Dopamine , noreepinephrine
• Thryroxine , insulin , steroids , vasopressin
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Kidney Transplantation
RENAL Transplantation;
• Most common indications are: Diabetes, glomeruronephritis
• Cadaveric and Living related TX.
• HLA is used in living related
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Complications of Renal Tx
• Arterial or Venous thrombosis.
• Ureter leak or stenosis
• Lymphocele 15%
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Question
• Three weeks after LRRT , a 35 years old male presents ipsilateral leg and abdominal wall edema and cyanosis of the leg . Normal kidney function. The most appropriate is
• A.Lower limb duplex and start Heparin
• B.Renal Ultrasound and biopsy
• C.Renal Ultrasound and Aspiration
• D.Renal Ultrasound and exploration
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• Ultrasonography is the first testRenal Biopsy for rejection
• US of transplanted kid can detect ;
• 1) Vascular anastomosis problems ( Artery or Vein)
• 2) Ureter anastomsis
• 3) Size of kidney(enlarged in rejection) or fluid collection around the kidney (lymphocele)
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• Causes of Oliguria after renal
Transplantation;
• A- Foley catheter blocked
• B- Arterial thrombosis
• C- Rejection (Acute or hyperacute)
• D- Acute tubular necrosis
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Question
• 5 weeks After CRT from a 60 years old healthy
donor, a 50 years old patient showed gradual rise
in Creatinine to 4,then remained stable. Renal US
normal. Renal Bx shows dilated tubules ,flat
tubular epithelium.The most likely explanation is
• Hyperacute rejection
• Acute rejection
• Acute tubular necrosis
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• Liver Transplantation
• The recipients are arranged according to the degree of illness (coma ,encephalopathy, coagulopathy., pulmonary hypertension)
• MELD; Model for End Stage Liver disease (0-40);less than 17 = no transplant yet
• Creatinine, bilirubin, INR ..
• Fulminating liver failure = immediate transplant
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Veno venous bypass (Anhepatic
phase)
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Adult to adult , use R lobe
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Adult to children < 5 years
segments 2 and 3
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• INDICATIONS OF Liver Tx;
• Liver failure from;
• 1) Hepatitis C is common
• 2) Non Alcoholic hepatic steatosis (NAHS) will be the most common
• . 3) Alcoholic Cirrhosis.
• 4) Sclerosing Cholangitis..
• 5)Biliary atresia in pediatric patients
• 6)Tumors ? Fibrolamellar carcinoma (Best prognosis) and some Hepatocellular carcinoma Stage I or II A in cirrhosis
Milan criteria ; if resection is not feasible for HCC liver transplant is good option for tumors less than 5 cm or 2 tumors 3 cm each . Patient is given a MELD of 22
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• It could be done with incompatible Blood
groups (results are mixed) and even in the
presence of preformed antibodies .
• Hyper acute rejection is rare with Liver TX
• Acute rejection occurs in 50 %
• Chronic rejection (vanishing bile duct
syndrome) is also common
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Complications of liver TX
• 1- Bleeding .(portal hypertension ,coagulopathy)
• 2- Portal vein thrombosis may go unnoticed
• 3- Primary Graft Nonfunction ? 2- 5% retransplantation
• 4- Biliary tract complications
• 5- Sepsis (most common cause of early death )
• 6- Hepatic artery thrombosis typically presents with bile duct stricture or leak.. Most require retransplants
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Pancreas Transplantation
• indication ;Diabetics
• Methods of TX
• Drainage of Duodenum into the urinary
bladder . Or into the small bowel
• Complications ;
• Vascular thrombosis
• Allograft pancreatitis
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Lung and Heart
• Lung transplantation ;
Broncholitis obliterans is the most common complication
Most lung transplants are unilateral .
In cystic fibrosis Bilateral lung transplant is needed to avoid infection in the new lung
Heart transplantation
Atheroslerosis of the new heart coronary arteries is the limiting long term complication
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New Immunosupressive drugs
mTOR inhibitor
• Normally Mtor is cell receptor which stimulates ;
• Cell growth and proliferation . Where mTOR regulates protein metabolism by ribosomes .
• mTOR also produce enzymes essential for glycolysis which is essential for cancer cells .
• mTOR also stimulates angiogenesis
• RAPAMYCIN (sirolimus) is the classic mTOR inhibitor (immunosuppresive – drug eluting stent – anticancer)
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New mTor inhibitor
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AFINITOR side effects
• Non infectious pneumonitis
• Viral bacterial infections
• Oral ulcerations
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• 3 years after renal Tx , a patient required distal
small bowel resection . He has been on steroids
and Cyclosporin ,he starts to develop rejection.
The most appropriate step is
• 1- increase steroids
• 2-start OKT3
• 3-increase cyclosporin
• 4-start antilymphocytic globulin
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• Question
• 10 years after renal TX ,a patient presents with
SOB ,Chest CT with 10 cm mid line opaque
lesion . The most appropriate is
• A.start antibiotics after culture,bronchoscopy
• B.Fine needle Aspiration
• C.Excision ,+ Chemotherapy
• D.Incision biopsy,+chemo
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APC
• Okt3 CD3
• CD4 Cyclosporin/
tacrolimus
• IL2
•
• CD8 mtor Sirolimus(rapamycin)