IMSE II Flashcards
LAD
____ protein DEFECTIVE. [component of adhesion receptors on [what cells: 3] ]
—Pathological consequence_________
—Laboratory Analysis manifestations ________
CD18
-Mono, Neutro, T-cell
-Abnormal VESSEL WALL adhesion + chemotaxis
–INC in Blood; [x] Infection site
Chediak Higashi Syndrome
____ _______ DEFECTIVE.
—Pathological consequence_________
—Laboratory Analysis manifestations ________
LYST, Phagosome-Lysosome
Recurrent pyogenic infection by Staph/Strep
Granulocytes/Platelets: Giant granules
Chronic Granulomatous Disease
________ DEFECTIVE for ____ killing.
—Pathological consequence_________
—Laboratory Analysis manifestations ________
Neutrophil’s inability to produce O2 REACTIVE FORMS
Bacterial
Abnormal Neutrophil Phagocytosis + Recurrent Infection
[X] NBT dye reduction
System that hinders Allogeneic Transplantation
Major Histocompatibility Antigens
Minor Histocompatibility Antigens
MHC Class I-related chain A [MICA]
ABO Blood group Antigens
Killer Immunoglobulin-like receptor System [KIR]
A system that hinders Allogeneic transplantation responsible for NK regulation
KIR system
transfer from a body part to another body part of same individual
Autograft
transfer from 1 twin to another twin
Syngeneic graft
transfer of cells/tissue between 2 individuals of the same species
Allograft
transfer of tissue bet. 2 individuals of different species
Xenograft
Pathways on how recipient’s immune system recognized foreign HLA proteins [2]
Direct Allorecognition
Indirect Allorecognition
Direct Allorecognition:
–MHC Type cells
–Requirements
– Response
MHC Class I
None
High frequency
Indirect
Allorecognition:
–MHC Type cells
–Requirements
– Response
MHC Class II
APC engulfment of MHC II foreign cells
Typical response
Hyperacute Transplant Rejection Type
– Onset
– Mediator
– End result [path. consequence]
– Prevention
Mins-Hrs after blood supply
HLA, ABO
Ischemia, Necrosis
INC. crossmatching sensitivity
Accelerated Transplant Rejection Type
– Onset
– Mediator
– End result [path. consequence]
– Prevention
after Several days
Very low levels: Donor-specific Ab [pretransplant period]
Ischemia, Necrosis
Proper crossmatching
Acute Transplant Rejection Type
– Onset
– Mediator
– End result [path. consequence]
– Prevention
Days-Weeks
Interstitial cells
Parenchymal, Vascular Injury
Immunosuppressive drugs
Chronic Transplant Rejection Type
– Onset
– Mediator
Weeks after transplant
Prolonged cold ischemia
Reperfusion
Acute Rejection episodes
Immunosuppressive drugs toxicity
cellular-type rejection but may ALSO involve AB hence name also called as “Acute Cellular Rejection’
Acute Transplant Rejection Type
Chronic rejection addt’l pathological consequence
–caused by
Graft arteriosclerosis [progressive fibrosis + scarring, vessel lumen narrowing]
Smooth muscle proliferation
special type of transplant rejection exclusive for stem cell, liver, lung transplant
Graft-versus-Host Disease
Graft-versus-Host disease mediator
Mature T-cells in donor blood
2 TYPES of Graft-versus-Host disease
ACUTE
CHRONIC
2 types of Acute Graft-versus-Host disease
- _______
[target of mature T-cell in donor’s graft] - ________
[target of mature T-cell in donor’s graft]
Mismatched Allogeneic Stem Cell Transplantation
-Mismatched HLA proteins
Matched Allogeneic Stem Cell Transplant
-Minor histocompatibility Ag
Occurs in first 100 days of stem cell/liver/lung transplant
Occurs in beyond 100 days of post-transplant
Acute Graft-versus-Host Disease
Chronic Graft-versus-Host Disease
Prevention for Chronic Graft-versus-Host Disease
Graft Irradiation
Graft removal of donor’s T-cell
3 IMMUNOSUPPRESSIVE AGENTS
Corticosteroids
Antimetabolic agents
Calcineurin inhibitors
act by blocking production/secretion of cytokines, inflammatory mediators, chemoattractants, adhesion molecules
Corticosteroids
interfere w/ lymphocytes’ maturation and kill proliferating cells
antimetabolic agents
blocks t-cells growth/diff. by impairing ____ synthesis
Calcineurin inhibitors
Cytokine
test for Phenotype in HLA Typing
Complement-dependent cytotoxicity test [CDC]
test for Genotype in HLA Typing
PCR-based amplification
study of antigens associated w/ tumors, immmune response to tumors, tumor’s effect on the host’s immune status, use of IS to help eradicate tumor
Tumor Immunology
regulatory genes that promote cell division
Protooncogenes
mutated protooncogenes
oncogenes
a tumor that doesn’t invade surrounding tissue and normal body function is largely preserved
Benign tumor
a tumor that invade surrounding tissue and body function is affected
Malignant tumor
where malignant cells travel through the body
Metastasis
Tumor dev’t stages
induction
In site
Invasion
Dessimination
________– carcinogen exposure + cells exhibit _____.
Induction
Dysplasia
neoplastic cells have formed but confined to the tissue of origin
In situ
cancer cells proceed only to invasion [adjacent organs/tissues] if they are malignant, not benign.
Invasion
traveling of malignant cells to the whole body through ____ and ______ _____.
Dissemination
blood, lymphatic vessels
Reasons for tumor/MALIGNANT cell GROWTH
TUMOR CELLS are:
1.poorly immunogenic
2.lack MHC molecules
3.resistant
4.growth rate > immune response
- Soluble ag [released by tumor] may bind to T-cell receptor = no interaction w/ tumor cell
- Gene mutations
higher amounts of antigens present in the tumor tissue than in normal tissue
they are tumor specific [True or False] [ if not, why?]
Tumor-associated antigens
False, tumor ag are also found in noncancerous human tissue
differential diagnosis of tumor type can be done by:
_________
_________
tissue/cell morphology
tumor markers directly from tumor tissue
Lab tests for tumor marker detection
1.Gross/Microscopic morphology of tumors
2. Antigen/Protein tumor markers detection
3. DNA/RNA molecular diagnostics
-Cytogenetic studies
-Nucleic acid amplification techniques [NAAT]
-Fluorescent in situ hybridization [FISH]
Ideal tumor markers
Produced by tumor
Secreted into biological fluid
Inepensive
INC in significant levels while disease is still treatable
Antigen must be ABSENT w/o malignant disease
Tumor marker class
Cell surface markers
Proteins
Oncofetal antigens
Carbohydrate antigens
Blood group antigens
Enzymes/Isoenzymes
Hormones
EXAMPLES of:
1. Cell surface markers
2. Proteins
3, Enzymes/Isoenzymes
4. Hormones
- Estrogen/Progesterone receptors
WBC CD markers - Thyroglobulin [TG]
IGs, Ig light chains [Bence Jones proteins]
3.
Prostate-specific antigen [PSA]
Alkaline phosphatase [ALKP]
Neuron specific enolase
- Human Chorionic Gonadotrophin
Calcitonin
Gastrin
EXAMPLES of:
1. Oncofetal antigens
2. Carbohydrate Antigens
3. Blood group antigens
- AFP
Carcinoembryonic antigen [CEA] - CA 125
CA 15-3 - CA 19-9 [Lewis antigens]
DISEASE Associations of:
1. Cell surface markers
2. Proteins
3, Enzymes/Isoenzymes
4. Hormones
1.
Breast cancer hormone therapy [prognosis]
WBC neoplasms [lineage/clonality]
2.
Papillary/Follicular THYROID Carcinoma
[well-differentiated]
Multiple MYELOMA
LYMPHOID malignancies
3.
PROSTATE cancer
BONE/LIVER cancer
NEURAL tissue neoplasms
- GERM CELL carcinoma
MEDULLARY THYROID cancer
PANCREATIC gastrinoma
TROPHOBLASTIC tumors
DISEASE Associations of:
1. Oncofetal antigens
2. Carbohydrate Antigens
3. Blood group antigens
1.
GERM CELL carcinoma
COLORECTAL carcinoma
HEPATOCELLULAR carcinoma
2.
Ovarian cancer
Breast cancer
- PANCREATIC cancer
GI cancer
transfer of antibodies, cytokines, or cells to patients who may not be able to mount an immune response
examples:
Passive immunotherapy
T cell
Antibody conjugates/immunotoxins
patients are treated in a manner that stimulates them to mount immune responses to their tumors
examples:
Active immunotherapy
Bacillus Calmette Guerin
Cytokines
Cancer vaccines
How do the bacteria evade the Immune System?
- Avoiding Ab [proteases’ destruction]
- Blocking Phagocytosis [M protein, No fusion of Granules and Phagosome]
- Inactivating complement casscade [Complement proteins’ disruption]
2 Phenomenons in Type 1 Hypersensitivity
- TH2 SWITCH response [normal th1 + th2]
- HLA molecules [allergen rxn in HIGH RESPONSE]
Type 1 Hypersensitivity
Time onset
Key reactant
Seconds-Minutes
IgE
Diseases associated with Type 1 Hypersensitivity
Atopy
Anaphylaxis
Rhinitis
Asthma
inherited tendency to respond to naturally occurring inhaled/ingested allergens w/ continued production of IgE.
Atopy
most severe type of allergic response
anaphylaxis
most common form of atopy/allergy
rhinitis
caused by particles not greater than 2-4 um. Greek word _____, ______.
Asthma
Panting, breathlessness
Diagnostic procedures for type 1 hypersensitivity
- ________________ test
-all IgE or Total IgE. Uses ______ labels. - ________________ test
-Ag-specific IgE. Uses ______ labels.
Radioimmunosorbent Test [RIST]
radioactive labels
Radioallergosorbent Test [RAST]
–enzyme of fluorescent labels.
Type I Hypersensitivity
–Also called as
–Mediator
–Effector cell
–Antigen involved
–Complement involved
–Mechanism
Anaphylactic/Atopic
IgE
Basophil, Mast cell
Allergen
NO
Release of inflammatory mediators
Type II Hypersensitivity
–Also called as
–Mediator
–Effector cell
–Antigen involved
–Complement involved
–Mechanism
Cytotoxic
IgM/IgG
RBC,WBC, PLT
Cell-bound Ag
YES
Cell lysis
Type III Hypersensitivity
–Also called as
–Mediator
–Effector cell
–Antigen involved
–Complement involved
–Mechanism
Immune Complex
IgM/IgG
Interstitial cells
Soluble Antigen
YES
Ag-Ab complexes deposition
Type IV Hypersensitivity
–Also called as
–Mediator
–Effector cell
–Antigen involved
–Complement involved
–Mechanism
Delayed/Cell-Mediated
T cell [TH1]
APC, Macrophage, T-cell
Sensitized Antigen
NO
Cytokines release
DISEASE EXAMPLE OF TYPE 1 HS
Anaphylactic:
Bee Sting
Food/Drug Allergens
Allergic/Atopic:
Asthma
Eczema
Hives
Hay Fever
rhinitis
DISEASE EXAMPLE OF TYPE II HS
AIHA
HTR
HDN
ITP
Goodpasture Syndrome
Rheumatic fever
DISEASE EXAMPLE OF TYPE III HS
Arthus reaction
Polyarteritis Nodosa
Poststreptococcal Glomerulonephritis
Serum Sickness
SLE
DISEASE EXAMPLE OF TYPE IV HS
Contact Dermatitis
GHVD
PPD
Poison ivy
