BY MUHAMMAD SAEED

Roll number , 46
MS.c BIOCHEMISTRY 3rd
Department of biochemistry
Baha uddin zakariya university
Multan pakistan
 The principle function of the immune system is
to protect host against pathogenic organisms
 Immunity maybe innate or specific
 Pathogens are defined as microbes capable
causing of host demage
 when host demage reaches a certain threshold
.it can manefist it self as a disease.
 pathogenic microorganism (bacterium, vir
us or protozoal parasite) infects the human
body, a battle ensures between the
host’s innate & adaptive immune
systems and cause some type of disease.
 Defence against pathogens is mediated by both
innate and acaquired immunity
 The innate immune response plays an
important role in determining the nature of the
specific immune system.
 Many pathogens also deploy diverse immune
evasion tactics in the host to achieve host cell
invasion and colonisation and may successfully
exploit host cells to access target.

 The survival and pathogenicity of pathogens in

a host are critically influenced by their ability
to evade or resist protective immunity.
 parasities

bacteria pathogens viruses

fungi
 The final subclass of infection is parasites
which are generally complex organisms which
invade through mucosal surfaces or the skin.

 Most effective strategy is to prevent infection

in the first place.

 Anaphylactic IgE mediated responses against

parasites evolved to prevent parasites from
entering to cell.
 The generation of IgE is dependent on the Th2
cytokine IL4. IL5 also secreted by Th2 cells recruits
eosinophils which can kill parasites by exocytosing a
cytotoxic protein, cationic basic protein.
 Th2 responses are maintained at mucosal sites by the
following mechanism
 . IL4 reinforces Th2 responses by inhibiting Th1 cell
development. Activation of mast cells which are
primarily located at mucosal sites and under the skin
leads not only to the release of histamine and other
inflammatory mediators which lead to expulsion of
parasites, but also IL4 secretion which reinforces the
local Th2 responses.
 Innate immunity is the first line of defense
against pathogens that invade human´s
organism and it´s mediated at the cellular level
by phagocytic cells including macrophages and
granulocytes
 Once the parasite interaction with host
receptors occurs, the innate immunity is
triggered.
 Macrophages and neutrophils phagocyte small-
size parasites and release cytotoxic factors to
destroy large parasites.
 After activation , macrophages and neutrophils
release a series of proinflammatory molecules
such as TNF, interleukin (IL)-1, chemokines,
and other mediators that promote growth and
differentiation of other immune cells such as
IL-12
 which activates the cytotoxic function of
natural killer (NK) cells and stimulates
interferon (IFN)-synthesis by T cells and NK
(triggering in this case Th1 responses).
 Granulocytes,
 granulocytes such as basophils, eosinophils and
mast cells have been implicated in the initial
production of Th2 cytokines such as IL-4 and
IL-13 .
 Natural Killer (NK) Cells ,
 These cells have two essential functions: (i) to
destroy abnormal or infected cells by cytotoxic
mechanisms similar to those used by cytotoxic
T lymphocytes and (ii) to release
proinflammatory cytokines and chemokines.
 T and B lymphocytes are the most
representative cells of adaptive immunity to
pathogens and therefore also to parasites.
 T lymphocytes expressing the TCR are troughly
divided into three subsets: CD4+ or T helper
(Th) cells, CD8+ or cytotoxic T lymphocytes
(CTL) and CD4+ regulatory T cells , although
the division is greater with the inclusion of
Th17 lymphocytes
 A dogma has been settled according to which Th1
responses are established to eliminate intracellular
pathogens .
 Th2 allow the elimination of extracellular
pathogens.
 . Thus, in general, the protective responses against
protozoa, many of them being intracellular, are
usually Th1 and are mediated primarily by IFN .
 while helminths, that are extracellular organisms,
need Th2 responses to be expelled and the key
cytokines are IL-4, IL-5 and IL-13
 Most of the parasites cause chronic infections,
with symptoms of low intensity, in order to
generate a lasting parasite-host relationship
and maximize the chances of transmission or
adapt the time to the biological process of its
life cycle.
 These pathogens have developed a variety of
mechanisms to adapt to the host, either by
evasion or modulation of the immune system.
 When parasites enter the host, they confront a
first line of defense: the innate immune system.
 . In many cases, the first contact occurs for
extracellular parasite forms with soluble factors
existing in the host, where the main effector is
the complement system.
 . One of the ways by which parasites achieve
complement inactivation is the acquisition of
complement regulatory proteins that are
anchored to their surface, such as glycoproteins
that accelerate the dissociation of the C3/C4b
convertase similarly to DAF proteins in host
cells.
 Parasites are able to avoid the effector
mechanisms of humoral and cellular adaptive
immunity.
 One mechanism by which parasites evade the
humoral response is through antigenic shift,
 Antigenic shift can occur among different
parasite stages.
 Parasites are complex organisms that have co-
evolved with their hosts, which have enabled
them to develop unique mechanisms to survive
within them and cause chronic infections.
 The effort made in recent years has paid off and
has permitted to describe many of the
mechanisms by which immune system reacts to
invading parasites and how parasites defend
themselves
 Thus, a new branch that studies the
relationship between the immune system and
the different parasites has been created.
 IMMUNE RESPONSE TO BACTERIA
 Immunity to bacterial infection is achieved by
means of anti body.
 two types of bacterial infection
 Intacellular
 Extracellular
 Extracellular bacteria cause disease by two
mechanisms.
 Many of these produce toxins and some cause
inflamation.
 IgG antibodies oposinze bacteria and enhance
phagocytosis.

 Antibodies neutralize bacterial toxins

 IgM and IgG activate the complement systems

 Intracellular bacteria have the ability to servive
and even replicate within phagocytes.
 Immune responses of intracellular bacteria are
very different from extracellular bacteria.
 Intracellular bacteria activate the natural killer
cells ,either directly or by stimulating the
macrophages production of IL 1,2 a power full
natural killer cell activating cytokine.
 Durring the innate immune response to intra
cellular bacteria phagocytes ingest and attemp
to destroy.
 Intracellular bacteria are resistant to
degredation within phagocytes.
 Intracellular bactreria activate the natural killer
cells either directly or by stimulating
macrophages production IL 12 powerful NK
activating cytokine.
 Viral infections directly stimulate the
production of INF.
 Interferons are antiviral protein or
glycoprotein produced by several type of cells
to viral infection.
 Natural killer cells lyes a wide variety of viral
infected cells.
 INF are in three types
 CELL MEDIATED IMMUNE RESPONSE,
 Most important in host defense , once a viral
infection is estiblished.
 CD8 and CD4 are the main component of cell
mediated antiviral defense.
 The immune mechanisms of defence against
fungal infections are numerous and range from
protective mechanisms that were present only
in innate immunity.
 Cell mediated immunity (CMI) is the main
mechanisms of defence.
 Th1 type is required for clearnce for fungal
infections.
 Th2 immunity usually required in
susceptibillity to infection
 Innate immunity recognize the infection very
rapidly.
 Once the fungi passed the physical barriers
they met with a series of defence mechanisms
including cellular membrane, cellular receptors
and several humoral factors.
 The host defence mechanism can adapt to
diffferent kinds of fungal infections.