IMSE II Flashcards by Sab Manlapaz

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

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Chediak Higashi Syndrome

____ _______ DEFECTIVE.
—Pathological consequence_________
—Laboratory Analysis manifestations ________

LYST, Phagosome-Lysosome
Recurrent pyogenic infection by Staph/Strep
Granulocytes/Platelets: Giant granules

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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

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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]

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A system that hinders Allogeneic transplantation responsible for NK regulation

KIR system

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transfer from a body part to another body part of same individual

Autograft

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transfer from 1 twin to another twin

Syngeneic graft

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transfer of cells/tissue between 2 individuals of the same species

Allograft

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transfer of tissue bet. 2 individuals of different species

Xenograft

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Pathways on how recipient’s immune system recognized foreign HLA proteins [2]

Direct Allorecognition
Indirect Allorecognition

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Direct Allorecognition:
–MHC Type cells
–Requirements
– Response

MHC Class I

None

High frequency

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Indirect
Allorecognition:
–MHC Type cells
–Requirements
– Response

MHC Class II

APC engulfment of MHC II foreign cells

Typical response

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Hyperacute Transplant Rejection Type
– Onset
– Mediator
– End result [path. consequence]
– Prevention

Mins-Hrs after blood supply

HLA, ABO

Ischemia, Necrosis

INC. crossmatching sensitivity

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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

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Acute Transplant Rejection Type
– Onset
– Mediator
– End result [path. consequence]
– Prevention

Days-Weeks

Interstitial cells

Parenchymal, Vascular Injury

Immunosuppressive drugs

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Chronic Transplant Rejection Type
– Onset
– Mediator

Weeks after transplant

Prolonged cold ischemia
Reperfusion
Acute Rejection episodes

Immunosuppressive drugs toxicity

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cellular-type rejection but may ALSO involve AB hence name also called as “Acute Cellular Rejection’

Acute Transplant Rejection Type

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Chronic rejection addt’l pathological consequence

–caused by

Graft arteriosclerosis [progressive fibrosis + scarring, vessel lumen narrowing]

Smooth muscle proliferation

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special type of transplant rejection exclusive for stem cell, liver, lung transplant

Graft-versus-Host Disease

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Graft-versus-Host disease mediator

Mature T-cells in donor blood

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2 TYPES of Graft-versus-Host disease

ACUTE
CHRONIC

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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

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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

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Prevention for Chronic Graft-versus-Host Disease

Graft Irradiation
Graft removal of donor’s T-cell

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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 5. Soluble ag [released by tumor] may bind to T-cell receptor = no interaction w/ tumor cell 6. 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

1. Estrogen/Progesterone receptors WBC CD markers 2. Thyroglobulin [TG] IGs, Ig light chains [Bence Jones proteins] 3. Prostate-specific antigen [PSA] Alkaline phosphatase [ALKP] Neuron specific enolase 4. Human Chorionic Gonadotrophin Calcitonin Gastrin

EXAMPLES of: 1. Oncofetal antigens 2. Carbohydrate Antigens 3. Blood group antigens

1. AFP Carcinoembryonic antigen [CEA] 2. CA 125 CA 15-3 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 4. 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 3. 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?

1. Avoiding Ab [proteases' destruction] 2. Blocking Phagocytosis [M protein, No fusion of Granules and Phagosome] 3. Inactivating complement casscade [Complement proteins' disruption]

2 Phenomenons in Type 1 Hypersensitivity

1. TH2 SWITCH response [normal th1 + th2] 2. 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 1. ________________ test -all IgE or Total IgE. Uses ______ labels. 2. ________________ 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