Immune Defence Mechanisms
Specific Defence
Inflammation
lecture from Physiology and Pathophysiology I
11. 10. 2022
M. Chalupová
Immune System
• system of defence against pathogens (bacteria, viruses, fungi,
parasites) and tumor cells
Nonspecific vs. Specific Defence
Congenital vs. Acquired Immunity
Congenital/Nonspecific Immunity Acquired/Specific Immunity
Congenital vs. Acquired Immunity
Surface Coverage
First Line of Defense
PHYSICAL FACTORS
• skin
• mucous membranes with lysozymes
• lacrimal apparatus
• salivary glands
• vaginal secretions
• flow of urine
CHEMICAL FACTORS
• sebum
• lysozyme
• gastric juice
• vaginal secretions
• urine
Nonspecific Immune System
Second Line of Defense
• generalized responses to pathogen infection – do not target a
specific cell type
Phagocytes
• neutrophils
• eosinophils
• macrophages
Non-phagocytic leucocytes
• basophils
• mast cells
Complement proteins
Complement
Specific Immune System
Third Line of Defense
HUMORAL (Ab-MEDIATED) IMMUNE SYSTEM
• antibodies
• B-cells (lymphocytes)
CELL-MEDIATED SYSTEM
• T-cells (lymphocytes)
• helper T lymphocytes (TH)
– produce and secrete chemicals that promote large numbers of
effector and memory cells
• cytotoxic T lymphocytes (TC)
– eliminate infected body cells and tumor cells
PHAGOCYTIC COMPONENTS
• macrophages, monocytes, neutrophils
• engulf foreign objects and inform T lymphocytes that a specific
antigen is present
Lymphocytes
Humoral (Antibody-Mediated)
Immunity
• production of antibodies by B-cells
• B-cells migrate to the lymphoid organs
(spleen, lymph nodes) after maturation
Antibodies
• synthesized by B-cells in soluble or cell-bound
form
• each antibody recognizes one specific antigen
• immunoglobulins (5 classes) – glycoproteins
• Ig G
• Ig M
• Ig A
• Ig D
• Ig E
Antibodies Structure
Antibodies Function
Antibodies Production
• polyclonal
• monoclonal
Primary and Secondary Antibody
Response
Antigen-Antibody Response
Cell-Mediated Immunity T-cells
Cell-Mediated Immunity T-cells
• T-cells recognize antigen associated with MHC
(major histocompatibility complex) molecules
in the cells
– MHC class I
– MHC class II
Cell-Mediated Immunity T-cells
TH helper cells
• TH cells receptors recognize antigen on the
surface of APC (macrophages)
• release of cytokines and activation of TC and
B-cells
• TC cells directly attack and destroy infected
cells CELL IMMUNE RESPONSE
• B-cells (plasma cells) produce antibodies
HUMORAL IMMUNE RESPONSE
Helper TH-cells
Cytotoxic TC-cells
• recognize the antigens on the surface of the
cells
• destroy infected cells (bacteria, viruses, fungi,
parasites), tumour cells, transplanted tissue
Cytokines
• small proteins involved in cell signaling
• amplify and regulate immune responses
• interleukins (IL-1, IL-2…)
• TNF-α (tumor necrosis factor alpha)
• INF-γ (interferon gama)
• colony-stimulating factors (G-CSF)
Complex Immune Reaction
• antigen ingested and presented by antigen
presenting cells (APC), like macrophages
• helper T-cells react with MHC-antigen complex
• T-cell activation, proliferation and cytokine
production
• cytokines activate other cells (macrophages, NK
cells, TC cells)
• IL-2 stimulates B-cells to be developed to plasma
cells with antibody production
Complex Immune Reaction
Inflammation
• defense reaction of the organism to injurious
stimuli
MAIN AIMS
• to neutralize and destroy invading and harmful
agents
• to limit the spread of harmful agents to other
tissues
• to prepare any damaged tissue for repair
Inflammation
Local Signs of Inflammation
FIVE CARDINAL-LOCAL SIGNS OF INFLAMMATION:
1. RUBOR (REDNESS)
2. TUMOR (SWELLING)
3. CALOR (HEAT)
4. DOLOR (PAIN)
5. FUNCTIO LAESA (LOSS OF FUNCTION)
…. - ITIS
Inflammation
Inflammation
SYSTEMIC MANIFESTATION OF INFLAMMATION:
• fever
• Increased leukocyte counts (leukocytosis)
• lethargy
• muscle catabolism
• increased acute phase proteins (CRP C-reactive
protein)
• increased erythrocyte sedimentation rate
(ESR/FW)
Inflammation
INFLAMMATION AND INFECTION ARE COMMONLY CONFUSED
BECAUSE THEY OFTEN COEXIST
INFECTION IS ALWAYS ACCOMPANIED
BY INFLAMMATION;
HOWEVER,
NOT ALL INFLAMMATION
INVOLVES AN INFECTIOUS AGENT
Inflammation
TISSUE DAMAGE and
RELEASE OF
VASOACTIVE and
CHEMOTACTIC
FACTORS
VASODILATATION
INCREASED
PERMEABILITY
NEUTROPHIL
EMIGRATION
PAIN REDNESS HEAT SWELLING SWELLING
Causes of Inflammation
Biological
• bacteria, viruses, fungi, parasites
Physical
• UV, temperature, X-rays
Chemical
• strong acids and alkalies
Endogenous
• autoimmune diseases, disintegrating tumor cells
Surgery, trauma