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Emil von Behring

Serum Antitoxin

Robert Koch

Cellular Immunity

Elie Metchnikof

Phagocytosis

Paul Ehrlich

Immunity

Charles Richet

Anaphylaxis

Jules Bordet

Complement

Karl Landsteiner
Macfarlane Burnet, Peter Medawar

ABO Blood Group (The Specificity and Serological


Reactions)
Discovery of Immunologic Tolerance

Gerald Edelman, Rodney Porter

Structure of Antibodies

Rosalyn Yalow

Radioimmunoassay

George Snell, Jean Dausset, Baruj


Benaceraf
Niels Jerne

Major Histocompatibility Complex

Georges Koehler, Cesar Milstein

Monoclonal Antibody

Susumu Tonegawa

Antibody Diversity

Edward Donnall Thomas, Joseph


Murray
Peter Doherty, Rolf Zinkernagel

Transplantation

Luc Montagnier, Francoise BarreSinoussi

Human Immunodeficiency Virus

Immunoregulation

Cytotoxic T Cell Recognition of virally infection

Lines of Defenses

Natural/Innate Immunity
-Standardized
-Acquired at birth
1st Line of Defense
Skin -- pH 5.6 (Lactic Acid)
-- Normal Flora: Staphylococcus epidermidis
--Competitive Exclusion- compete with pathogens
Secretions
Lysozyme and Muramidase
Mucous Membrane
IgA
Vagina- Lacto acidophilus; duodelus
Gastric pH 1-2
2nd Line of Defense
1. WBC
2. Complement
3. Interferon
4. Interleukin
5. Tumor Necrosis Factor
6. Betalysin
7. Properdin
1. WBC
Neutrophil (60-70)
Eosinophil (1-3)
Basophil (0-1)
Mast Cell Tissues
Monocyte
Macrophage- Tissues

WBC

CirculatingMarginating ----Diapedesis
Pool
Tissue
Blood
50%
50%
*Selectin- makes neutrophil

sticky
Neutrophil
- Polymorphonuclear
- 3-5 segments
- 1st cell to arrive at the site of infection within 30-60 minutes
- duration to the site of about 16-24 hours

Predominant cell in acute inflammation


Phagocytic together with monocyte

Granules:
Primary/ Promyelocyte/ Azurophilic / Non Specific
Enzymes:
Myeloperoxidase
Elastase
Proteanase 3
Lysozyme
Cathopsin
Defensin
Secondary/ Myelocyte/ Specific
Enzymes:
Collagenase
Lysozyme
Lactoferrin-salvage of iron para di magamit ng bacteria
NADPH Oxidase
Other CHONS associated with Plasma Membrane
Tertiary Granule
Enzymes:
Gelatinase
Plasminogen Activator- Plasmin Fibrinolysis
Eosinophil
- Parasitic
- Homeostatic regulator of inflammation
Granules:
Primary
ACP
Aryl sulfatase
Secondary
MBP- Major Basic Protein
Kill parasite*
Charcot- Leyden Crystal
Trichinella Spiralis
Orange
Phagocyte but less efficient
Basophil
- Basophil- Blood : Mast Cell- Tissue
- Allergies / Hypersensitivity Type I/ Anaphylaxis
- Histamine and Heparin
- Mast CellParenchymal origin
Proteanase
Aryl sulfatase
ACP
Monocyte
- 1-10% blood: Macrophage- tissue

Largest in peripheral blood smear


NucleusHorse Shoe
CytoplasmGround Glass Appearance
Move to the site of injury within 4 hrs ( go back to Neutrophil and compare)
Peak hours 16-24 hrs
Duration of 48 hrs
Predominant Cell in Chronic Inflammation
MACROPHAGE:
Liver-Kupfer Cell
CNS- Microglial Cell
Lungs- Dust Cell (Bryant); Alveolar (Stevens)
Spleen- Littoral (Bryant); Splenic (Stevens)
Kidney- Mesangial Cell
Placenta- Hofbauer
2. INTERFERON
Virus-Non specific
Host- Specific

Type I Alpha: Leukocyte Interferon


Producers- virally induced leukocyte culture
Major producer- Null Lymphocytes
NK Cell- Large granular lymphocyte
Clinical Implication: Treatment for Hepa C
Kaposis Sarcoma- present in AIDS HSV-8
Type I Beta: Fibroepithelial Interferon
Producers- dsRNA induced and Fibroblast cultures
Major Producers- Fibroblast and Epithelial Cell
Clinical Implication: Multiple Sclerosis
Type II Gamma- Immune Interferon
Producers- Antigen/ Mitogen stimulated lymphocyte culture
Major Producer: T- Cell
3. INTERLEUKIN
Acute Phase Reactants- IL6
-pro inflammatory proteins
-Increase in inflammation
Types:
Positive Acute Phase Reactants- Non specific
-Indicator of inflammation
1. CRP C-reactive Protein
- Ab to C protein of Pneumococci *Cardiovascular Dse(female) CRP-Beta
-Function: OPSONIN- to prepare for eating
2. SAA Serum Amyloid A
- taga linis ng mga kalat ng phagocytosis
-same HDL
- bacterial than viral
3. AAT Alpha Anti-Trypsin
-Proteanases( Elastase)
Clinical Implication- Emphysema- absence of AAT
4. MBP Mannose Binding Protein *Clinical Implication: Recurrent Infection; Fungal
and Yeast Infxn
Ceruloplasmin-binds to Copper

-present in Alpha2 region


Clinical Implication: Wilsons Dse- Absence of Ceruloplasmin
Haptoglobin- Binds to Free Hemoglobin to prevent going to kidney
- Free Hgb( Lyse) and damages the kidney
- present in Alpha2 region
-Intravascular Hemolysis Haptoglobin
Fibrinogen- Beta region

Negative Acute Phase Reactants


-Decrease Albumin (analyte) if there is infection
-Level of Dehydration and Osmotic Regulation
Clinical Implication: Nephrotic Syndrome
Disease and Infection
Albumin
*IL-1 Mediator of Inflammation
Produced by Activated Macrophage
*IL-8Second Mediator of Inflammation
Pro-inflammatory

4. BETALYSIN
-Heat Stable Cationic substance produced by Platelet against Gram (+) bacteria except
streptococcus
5. PROPERDIN
-Part of Complement in Alternative Pathway
NEEDS: C3 and Mg2+
6. TUMOR NECROSIS FACTOR
- Mediator of Natural and Adaptive Immunity
-Mediator of Gram (-) Bacteria
TNF- produce Endotoxin
Clinical Implication: Septic Shock
2 Types of TNF:
TNF Alpha CACHETIN
-macrophage

TNF Beta LYMPHOTOXIN


- CD4 & CD8 Cells

Adaptive Immunity
-

Specific
Not acquired at birth
Not standardized

1. Humoral
B-Cell Plasma Cell Antibody
Exogenous
2. Cellular
T-Cell
Endogenous

ACTIVE

NATURAL
Infection

ARTIFICIAL
Vaccination

PASSIVE

Colostrum ( IgA)

Ig Administration

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