The document defines immunity and distinguishes between innate and adaptive immunity, outlining their characteristics and components. It provides an in-depth explanation of the complement system, its activation pathways, and the roles of various proteins in pathogen clearance and inflammatory responses. Additionally, it discusses complement deficiencies and their clinical manifestations, highlighting their association with conditions like systemic lupus erythematosus and glomerulonephritis.

1. Immunochemistry

2. Definition:
 Resistance of the body against the
pathogenic agents is known as
immunity

3.  Immunity is of two types:
 (i) Innate immunity
 (ii) Adaptive immunity

4. Differentiation
Characteristics Innate immune
system
Adaptive immune
system
Synonym Non-specific
(without antigen
specificity)
Specific
(characterized by
Antigenic
specificity)
Found in
organism
In all living
organisms
Vertebrate only

5. Characteristics Innate immune
system
Adaptive immune
system
Components First line defense:
- Epithelial barriers
that block entry
of microbes
- The enzymes of GIT
and HCl in the
stomach (destroy
the toxic
substances from
food)
- “Lysozymes” in
saliva, nasal
secretion, tears,
etc.
-Wax in ears
Antigen-presenting
cells (APCs)
Definition:
APCs are defined
as cells, which
have highly
specific receptors
for antigen

6. Characteristics Innate immune
system
Adaptive immune
system
Humoral
Components
(refers to body fluid)
-Complement
factors
-Cytokines
-Acute phase
proteins
-WBCs
B-lymphocytes
(B-cells)
Immunoglobulins
(antibodies)
Cellular components
(refers the cells)
-NK (natural
killer) cells,
-Micro- and
macrophages
T-lymphocytes
(T-cells)

7. What is Complement
system?

8.  Definition:
 The complement system is a set of
plasma proteins that help the ability
of antibodies and phagocytic cells to
clear pathogens from an organism.
 4% of all plasma proteins are
complement proteins, that are
numbered as C1, C2….. C9.

9. Where complement proteins are
synthesized?
 Complement proteins
are synthesized by:
 Liver hepatocytes
 Tissue macrophages
 Blood monocytes
 Epithelial cells of
genitourinal tract and
gastrointestinal tract

10.  Complement proteins present in the
blood in inactive form.
 Activation of proteins is result of
proteolytic cleavaged by convertases.
C3 convertase
C3 C3aC3b +
active subunits
inactive
C5 convertase
C5 C5b C5a+
active subunits
inactive

11. Three ways of activation
Classical
pathway
Alternative
pathway
Lectin
pathway
Antibody independentAntibody
dependent
generation of protease
C3 convertase
caSCADE
activation
of complement factors
EFFECTS
C5 convertase

12. Classical pathway of
complement activation

13. Initiators of Classic pathway
 Immunoglobulin-antigen complex
 C1 protein exist in blood serum as a molecular complex
containing:
 6 molecules of C1q
 2 molecules of C1r
 2 molecules of C1s
S S
R R
binds with IgM or
IgG (CH2-region)
activation
of C1r and C1s
When C1q1.
2. 3.C4
C4b + C4a
Activation of C4 and C2C2
C2b + C2a
C4b-C2b
C3 convertase
C3
C3b + C3a
C4b-C2b-C3b
C5 convertase
C5
C5b + C5a

14. Alternative pathway of
complement activation

15. Alternative pathway of
complement activation
 A pathway of complement activation
initiated by
 Bacterial endotoxins,
 Microbial polysaccharides,
lipopolysaccharides,
 Microbial cell walls
 Factors: B, D (adipsin)
 Stabilization of C3-convertase: Factor P
(properdin)

16. Complement activation cascade
C3
B
C3 Bb
Ba
C3
C3b
C3a B
C3b
1
2 3
Bb
P
D
c3 convertase
4
C3
C3b
Bb
P
C3b
c5-convertase
C5
C5b
C5a
5
6
C3a
exotoxin
of bacteria
wall of bacteria

17. Mannan-binding lectin
pathway (Lectin pathway)

18.  It activates complement through the
mannose-binding lectin (MBL) which
is produced by the liver and can
initiate the complement cascade.
 MBL binds to specific carbohydrates
(fucose, mannose) found on the
surface of many pathogens.

19. MBL binds with
 Yeasts such as Candida albicans
 Viruses such as influenza A, HIV
 Many bacteria such as Streptococci,
Salmonella
 Parasites like Leishmania

20. Bacteria
mannose
or fucose
MBL
MASP
C2
C2b
C2a
C4
C4b
C3 convertase
C4a
MASP - Mannan-binding lectin-Associated Serine protease
C3
C3b + C3a

21. Effects of activated complements
Effects of
C3a and C5a
Effects of
C3b and C5b
Produce inflammatory
mediators
Opsonization (C3b)
Formation of MAC
(complement fixation)
(C5b)Chemotaxis

22. Opsonization (Greek: “ to prepare
for eating”)
 Opsonization- is the
process of coating the
pathogens and
preparing them for
phagocytosis.
 Opsonins- substances
that bind a microbe to a
phagocyte and promotes
phagocytosis.

23. C3b is important opsonin. C3b is
riched by thioester groups which
react with –OH or -NH2 groups.
NH2
bacterial
membrane
S C
O
NH
SH C
O
Phagocytes
may recognize
this complex

24. MAC (membrane attack complex)
formation

25. BIOLOGICAL ROLE
C3a / C5a
 INFLAMMATORY RESPONSE
 C3a and C5a activate releasing of
HISTAMINE by mast cells, basophiles
and platelets.
 C3a and C5a activate leukocytes

26. Effect of histamine
 Vasodilatation (increase in the
diameter of blood vessels, especially
arteries).
 Increases vascular permeability and
hence increases migration of plasma
proteins (active complement,
cytokines, leukocytes) into the tissue
for pathogen inactivation.

27. CHEMOTAXIS

28. COMPLEMENT DEFICIENCIES
 Classic and
alternative pathways
complements
deficiency:
Clinical signs:
(i) Pyogenic (causing the
formation of pus)
infections
(ii) Immune-complex
syndrome**

29. MAC formation complement
deficiency
 Clinical signs
Immune-complex
syndrome**

30. Immune-complex
syndrome
 Include:
(i) SYSTEMIC LUPUS ERYTHEMATOSIUS
(SLE) – chronic inflammatory disease of
connective tissue, affecting the skin,
kidney, lungs, heart, brain (eg. formation
of fibrous scar)
(ii) GLOMERULONEPHRITIS- group of
kidney diseases involving the glomeruli
(iii) VASCULITIS – inflammation of the walls
of small blood vessels