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Immunological Diseases. Spectrums and Mechanisms Assistant Professor Kiat Ruxrungtham, M.D. Division of Allergy and Clinical Immunology Department of Medicine, Faculty of Medicine Chulalongkorn University. Principles of Immunology. Key roles of immune responses Terminology

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immunological diseases

Immunological Diseases

Spectrums and Mechanisms

Assistant Professor Kiat Ruxrungtham, M.D.

Division of Allergy and Clinical Immunology

Department of Medicine, Faculty of Medicine

Chulalongkorn University

principles of immunology
Principles of Immunology
  • Key roles of immune responses
  • Terminology
  • Primary and Secondary Immune Responses
  • Cells and Molecules involved
  • Immunological Disorders
  • Mechanisms and Clinical Implications
key roles of immune system
Key Roles of Immune System
  • Prevent and control infection
  • Prevent and control autoimmune diseases
  • Prevent and control malignancy
  • Prevent and control allergic diseases
  • Prevent and control graft-versus-host (GVH)
terminology
Terminology
  • Antigen, allergen, immunogen and epitope
  • Innate and Acquired Immunity
  • Allergy
  • Autoimmunity, autoimmune diseases
innate and acquired immunity
Innate and Acquired Immunity

Innate Acquired

Ag specificity no yes

Magnitude (10, 20) same higher (20 > 10)

Memory no yes

Key components PMN, NK T, B lymphocytes C’, barriers APCs

primary and secondary immune responses
Primary IR

7-10

relatively low

Mostly IgM

relatively high

Secondary IR

2-5 days

relatively high

Other class (IgG, IgA, etc)

relatively low

Primary and Secondary Immune Responses

Lag period

Peak response

Ig class

Antigen [ ]

cells and molecules involved in immunology
Cells and Molecules Involved in Immunology

Innate Immunity

  • Cells: epithelium, phagocytes (neutrophils, monocyte-macrophages) NK cells, mast cells
  • Molecules: complement, inflammatory mediators, cytokines, chemokines, adhesion molecules
cells and molecules involved in immunology8
Cells and Molecules Involved in Immunology

Acquired Immunity

  • Cells: APCs (macrophages), T (CD4+, CD8+) and B lymphoctyes (plasma cells), monocytes
  • Molecules: HLA, cytokines, immunoglobulins, adhesion molecules
immunological disorders
Immunological disorders
  • Hypersensitivity mediated disorders
  • Immunodeficiency : 10 and 20 ID
classification of hypersensitivity
Classification of Hypersensitivity

Gell and Coomb’s Classification: 4 Types

  • Type 1 : IgE-mediated
  • Type 2 : Cytotoxic antibodies
  • Type 3 : Ag-Ab Immune complexes
  • Type 4 : Delayed-type, cell-mediated hypersensitivity
type i hypersensitivity
Type I Hypersensitivity
  • Allergen exposure, sensitization and re-exposure
  • IgE antibody, mast cells/ basophils and its’ mediators
  • Target organ immediate reactions
  • Clinical allergy: atopic diseases, drug allergy, insect allergy and anaphylaxis
pathogenesis of allergic disease
Pathogenesis of Allergic Disease

Genetic Susceptibility

  • Adjuvant factors:
  • Tobacco smoke
  • Air pollutants
  • Lack of protective
  • factors:
  • Infection ?
  • Immunization ?
  • Nutrition ?

Allergic Sensitzation

Allergen

Exposure

Upper/lower airway or Skin

hyperresponsiveness

Pollutants

Infection

Excercise

Vary in spectrum

and severity

Allergic Diseases

Modified from Ulrich Wahn 1998

principle pathogenesis of allergic diseases
Principle Pathogenesis of Allergic Diseases

Durham and Till 1998, Lu 1998, Drazen 1996

APC

Allergen

CD4+ T-cell

IL-12

Allergen

Th-1

Th-2

IL-4

IgE

IFN-g

IL-5

IL-3

GM-CSF

B-cell

B-cell

CD8+ cell

IgG

Mast

cell

IL-5

Other cells

_

+

Eosonophil

MBP

ECP, LTs

Late Phase Reaction

Tryptase, LTs

AllergyChula

slide14
Pathogenesis of

Allergic Diseases

Cells & Molecules

Involved in

Allergic

Inflammation

Modified from

Robert Davies

mediators of mast cells and basophils
Histamine

Tryptase

Chymotryptase

Heparin/Chondroitin

Kininogenase

Chemotactic Factors

Prostaglandins

Leukotrienes

PAF

Histamine RFs

IL-3, 4, 5, 6, 7, 8

GM-CSF, TNFa

Chemokines -MCP1, MIP1

Oxygen radicals

Mediators of Mast Cells and Basophils

Secondary Mediators

Primary Mediators

AllergyChula

Sim TC, Grant JA 1996

mediators of mast cells and allergy
Mediators of Mast Cells and Allergy

Urticaria, Angioedema

Laryngeal edema, Shock

Blood Vessels

H, PGD2,

LTs, PAF

Kinin

Bronchospasm

Abd. pain, Vomiting

Smooth Muscles

H, PGD2,

LTs, PAF

Diarrhea, Rhinorhea

Bronchial secretion

Mucus Glands

H

Mast Cell

Basophil

Sensory Nerves

Itching

LTB4

PAF

IL3, IL5

Chemokines

Leukocytes

Inflammation - LPAR

AllergyChula

slide17
โรคภูมิแพ้ที่พบบ่อย

โรคภูมิแพ้ทางจมูก Allergic Rhinitis

โรคหืดจากภูมิแพ้ Allergic Asthma

โรคภูมิแพ้ทางผิวหนัง Atopic Dermatitis

โรคลมพิษUrticaria

โรคแพ้อาหาร Food Allergy

การแพ้ยา Drug Allergy

Allergy Chula 1999

epidemiology of allergic diseases in thai children
Epidemiology of Allergic Diseasesin Thai Children

พยนต์ บุญญฤทธิพงษ์ และมนตรี ตู้จินดา 2533; ปกิต วิชยานนท์ และคณะ 2541

slide20
สิ่งแวดล้อม กับ โรคภูมิแพ้

ฝุ่นบ้าน

ฝุ่นบี่นอน

สัตว์เลี้ยง

เชื้อรา

เกสร

ที่กักฝุ่น

อาหาร

ตัวไร่ฝุ่น

สิ่งเหล่านี้มีอยู่รอบตัวเรา มีทั้งในบ้านและนอกบ้าน

แต่มีหลายอย่างที่เราหลีกเลี่ยงได้ หากเรารู้วิธีที่ถูกต้อง

slide21
ควันบุหรี่

ควันธูป

factors affecting clinical outcomes of allergic diseases
Factors Affecting Clinical Outcomesof Allergic Diseases
  • Treatment
  • Anti-inflammatory
  • Anti-allergic
  • Relievers
  • Enivronmental
  • Allergens
  • Irritants
  • Westernization

Genetic

Degree of atopy

  • Compliance
  • Avoidance
  • Medication uses
  • Infection
  • Viral
  • Bacterial

Allergen

Immunotherapy

Allergic Diseases

Future Therapy ?

Remission

Mild

Severe

Moderate

AllergyChula

clinical uses of h 1 antagonists
Clinical Uses of H1 Antagonists

Generation of Antihistamines

Clinical First Second and Third

Allergic Rhinitis ++ ++ (better compliance)

Urticaria ++ ++ (better compliance)

Atopic dermatitis ++/+++ ++ (better compliance)

Asthma - -/++(Meta-analysis= NS)URI/NAR ++ -

Itching dermatosis ++/+++ ++

Anti-motion sickness ++ -

Antiemetic ++ -

Appetite stimulation ++ -(+ for astemizole)

Insomnia ++ -

AllergyChula

treatment of allergic asthma
Treatment of Allergic Asthma

Allergy 1994; suppl. 19

type ii hypersensitivity
Type II Hypersensitivity
  • Cytotoxic antibodies: IgG, IgM
  • Mechanisms of cytolysis: Fix complement and/or ADCC
  • Clinical spectrums:
    • Autoimmune Hemolytic anemia (AIHA)
    • ABO Miss-matched
    • ITP
  • Stimulatory antibody: Grave’s disease
  • Inhibitory antibody: Myasthenia gravis (anti-Ach Rc)
principle treatments in type ii
Principle treatments in Type II
  • ABO matching
  • For AIHA, ITP: Steroid, immunosuppressive agents, +/- splenectomy
type iii hypersensitivity
Type III Hypersensitivity
  • Mechanisms: Ag (protein, drugs) + Ab (IgG, IgM) --> Immune complex --> deposit at subendothelial basement membrane --> fix complement --> chemotaxis ---> PMNs --> vasculitis
  • Immune complex diseases:
    • Serum sickness
    • Autoimmune diseases: prototype-SLE
    • Vasculitis
principle treatments in type iii
Principle treatments in Type III
  • Serum sickness: Avoidance of heterogeneous protein injection: ERIG antirabies
  • Autoimmune diseases: SLE
    • Avoidance sun exposure
    • Steroid
    • Immunosupressive agents
type iv hypersensitivity
Type IV Hypersensitivity
  • Delayed-type cell-mediated reaction
  • Mechanism: Antigen (contactants) --> sensitized T-lymphoctyes --> re-exposure --> T cells activation --> cytokines ---> mononuclear cell recruitment --> DTH
  • Clinical disorder: Atopic contact dermatitis
principle treatments in type iv
Principle treatments in Type IV
  • Avoidance
  • Topical steroid
  • Systemic steroid, if severe
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