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Hypersensitivity Reactions, a Type of Immune Response

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 RESEARCH TRENDS
N
MED CAL SCIENCES
Volume - 20

Chief Editor
Sergiy Fedorov (MD, Ph.D., MBA, D.Sc.)
Professor of Therapy and Family Medicine, Department of Postgraduate
Faculty, Ivano-Frankivsk National Medical University, Ukraine

AkiNik Publications
New Delhi
Published By: AkiNik Publications

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Publication Year: 2022
Pages: 138
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Price: ` 748/-
 Contents

Chapters Page No.

1. MR Imaging in Mucormycotic Rhinosinusitis 01-19
(Dr. Pooja M, Dr. Prashant Titare, Dr. Varsha Rote Kaginalkar, Dr. Ajay Vare,
Dr. Anjali Pawar and Dr. Majed Khan)

2. Feeding and Eating Disorders 21-35

(Dr. Irina Pîrvan, Psih Alexandra Geară and Dr. Simona Trifu)

3. Hypersensitivity Reactions, a Type of Immune Response 37-56

(Dr. S. Anu Kiruthika, Qurath Ul Ain, Bawanshisha Syiemlieh and NB Karthik)

4. The Depressive Disorder and the Endocrine System-Holistic

Perspective 57-76
(Virginia Corduneanu, Dr. Cătălin Ragia and Dr. Simona Trifu)

5. Somatic and Related Symptom Disorders 77-88

(Cristina Andronache, Alina Marina Marian, Ilinca Vlaicu and Simona Trifu)

6. Pharmacological Properties of Acacia nilotica L: A Review 89-104

(Dr. Sheik Nasar I)

7. An Updated Review on Atherosclerosis Reflation: Past Insight

and Future Research Directions 105-130
(Akshita G. Bhanderi and Megha Gandhi)

8. Bilateral Adrenal Myelolipoma: Imaging Features 131-138

(Dr. Vasudha Nikam and Dr. Niranjan Patil)
 Chapter - 3
Hypersensitivity Reactions, a Type of Immune
Response

Authors
Dr. S. Anu Kiruthika
Associate Professor, Department of Microbiology, Indian
Academy Degree College Autonomous, Bengaluru, Karnataka,
India
Qurath Ul Ain
M.Sc. Students, Department of Microbiology, Indian Academy
Degree College Autonomous, Bengaluru, Karnataka, India
Bawanshisha Syiemlieh
M.Sc. Students, Department of Microbiology, Indian Academy
Degree College Autonomous, Bengaluru, Karnataka, India
NB Karthik
M.Sc. Students, Department of Microbiology, Indian Academy
Degree College Autonomous, Bengaluru, Karnataka, India

Page | 37
 Chapter - 3
Hypersensitivity Reactions, a Type of Immune Response
Dr. S. Anu Kiruthika, Qurath Ul Ain, Bawanshisha Syiemlieh and NB Karthik

Abstract
Hypersensitivity is the exaggerated immune response to protect the
human from foreign bodies known as antigens. Hypersensitivity reactions may
lead to various consequences ranging from mild symptoms to severe shock
causing death. Hypersensitivity can be classified into four types; namely, type
I (Immediate), type II (Antibody-mediated), type III (Immune complex-
mediated), and type IV (Cell-mediated or Delayed-type) hypersensitivity.
Each type of hypersensitivity reaction is an extreme immune response to an
antigen. Each type of reaction differs based on the type of antigen the body
identifies. A hypersensitivity reaction describes the immunological process
that occurs in the body.
Keywords: Hypersensitivity, immune response, antigen, antibody, allergen,
immune-complex and reaction
Introduction
Hypersensitivity is defined as an immunological state where immune
response is produced by immune system against antigen. It can also be referred
as an excessive, unwanted immunological reactions taking place towards
antigen by immune system. This immune response in turn invites and
mobilizes different effector molecules that induce inflammatory response
locally. Generally, inflammatory response does not damage the tissue of the
host in great extent but in some cases, it shows deleterious effects like
significant damage to the tissues and even death (Yalew ST., 2020). After the
first exposure of host to an antigen, the host becomes hypersensitive to that
specific antigen and therefore can fight against it in second exposure (T.V.
Rajan., 2003).
Drug hypersensitivity reaction is defined as an immune response specific
to the drug that act has a hapten, that is directed against a hapten carrier
complex. This hapten carrier complex is considered as an allergen. (Pychler.
J. w., et al., 2019). Hypersensitivity that is caused by non-Ige mediated after

Page | 39
the introduction of nano medicines through intravenous is rare but has
significant effect such as, liposomal doxorubicin (Fulop. T. et al., 2019). Drug
hypersensitivity reaction is caused by adverse drug reactions however it is
shown by only 15% of cases.it is the third reason of allergy because of
significant increase in its existence over last years (Mayogra. C., et al., 2019).
Clinically, drug hypersensitivity reactions are categorized into two, the
former is immediate reactions which takes place within 1 to 6 hours after
administration of drug and causes angioedema, urticaria, and the latter is no
immediate reactions which occurs after one day of drug administration and
causes maculopapular exanthema, Stevens -Johnson syndrome drug reaction
with eosinophilia and systemic symptoms, abasabir hypersensitivity syndrome
etc. (Mayorga. C., et al., 2019). Type A reaction is ca used mainly by drug
hypersensitivity. Type B reactions are and shows only 15% of drug
hypersensitivity. (Pychler. J.W., et al. 2019).
Hypersensitivity reactions takes place by during anesthesia remain major
cause of treat for anesthesiologists. Dissension still continue Concerning
possible with difference regarding the parallel risk of allergic reaction and
among neuromuscular blocking agents. (S.W. Dong., et al., 2007).
Hypersensitivity is identify by the short sharp pain from exposed dentine in
reaction to stimuli typically thermal, tactile, evaporative, osmotic, and which
cannot be ascribed to any other form of dental pathology. Dentinal
hypersensitivity can appear through erroneous gingival recession,
toothbrushing, because of other factors. It is maintain that 14.3% of all patients
have some degree sensitivity. (Dowell., et al., 2000).
Hypersensitivity reactions can be broadly manifested into two types
a. Immediate hypersensitivity
 Immediate hypersensitivity is also referred to as humoral
hypersensitivity.
 Occurs within a few minutes after the antigen combines with its
antibodies.
 It involves antibodies against antigens of pathogens or tissue
reactions.
b. Delayed-type hypersensitivity (DTH)
 Delayed type hypersensitivity is commonly known as Cell-mediated
hypersensitivity.
 Occur after an hour of exposure to an antigen and can take 1-3 days
to manifest themselves.

Page | 40
  Not only produces antibodies against processed antigens but also
increases the sensitivity of T-Lymphocytes against this specific
antigen for future interactions (Ajoy Paul, 2016).
Types of hypersensitive reactions
In 1963, Phillip Gel and Robert Coombs classified the hypersensitivity
reactions into four types based on the extent of damage caused due to the over-
reaction in the parts of the immune system.
These are:
1) Type I hypersensitivity reactions (Anaphylaxis).
2) Type II hypersensitivity reactions (Antibody-dependent
cytotoxicity).
3) Type III hypersensitivity reactions (Immune complex-mediated
hypersensitivity).
4) Type IV hypersensitivity reactions (Delayed Type or Cell-mediated
hypersensitivity).
5) Type V hypersensitivity reactions (stimulatory hypersensitivity).
Out of these four types, the first three types of hypersensitivity reactions
fall under Immediate Hypersensitivity reactions whereas Type IV comes
under Delayed-type hypersensitivity reactions (Shyamasree Ghosh, 2017).
1. Type I hypersensitivity reactions (Anaphylaxis)
 Type I hypersensitivity reactions also known as immediate or
anaphylactic hypersensitivity occur within 15-30 minutes and
sometimes 6-8 hours from the time of exposure to the antigen (Yalew
ST, 2020).
 These are IgE mediated immune responses which commonly include
allergic reactions such as allergic rhinitis (hay fever), asthma,
eczema, food allergies, etc. this reaction is initiated when the IgE
antibodies interact and react with the multivalent antigens. During
the 1960s-1970s, K Ishizaka and T Ishizaka identified IgE as a class
of antibodies responsible for allergies (Jenny Punt, 2019).
 The primary cellular components involved in Type-I reactions are
mast cells and basophils, the response is amplified and additionally
modified by platelets, neutrophils, and eosinophils (Yalew ST, 2020)
(Punt, 2019).
 The antibodies which strongly adhere to the tissues specifically to the
mast cells in the tissues are termed "Tissue sensitizing antibodies"

Page | 41
 and are capable of inducing anaphylactic type-I reactions.
Anaphylactic reactions are caused by antigen-antibody reactions on
the surface of the mast cells, activating a series of enzymes leading
to the release of histamines and other agents from the mast cells
(Ajoy Paul, 2016).
A. Etiology of type-i hypersensitivity
Type-I hypersensitivity reactions against the antigen occur in two phases:
The sensitization phases
In this phase, the host encounters an asymptomatic contact with the
antigen.
The impact phases
In this stage, the pre-sensitized host is re-introduced to the antigen which
leads to type-I anaphylactic or atopic immune responses (Malak Abbas, 2021).

Mechanism of type-i hypersensitivity reactions

 The immunological basis of this hypersensitivity is the cytotropic IgE
antibody. There are basically two types of IgE receptors: - the high-
affinity receptor (FcERI) mainly found in large numbers on the
surface of mast cells and basophils and the low-affinity receptor
(FcERII or CD23) found on NK cells, macrophages, dendritic cells,
eosinophils, and platelets (Ian R. Tizard, 2007).

Page | 42
 The IgE molecules with the help of its FC region, binds to these high-
affinity surface receptors (FcERI) which are analogous to the TCR
receptors present on the surface of T cells.
 Furthermore, exposure to the shocking dose, the antigen molecules
combine with cell-bound IgE, thereby bridging the gap between
adjacent antibody molecules. This cross-linking increases the
permeability of the cells to calcium ions and leads to degranulation
and hence releases biologically active substances contained in the
granules (Reba Kanunga, 2017).
 The release of immunomodulators also known as mast cell
degranulation stimulates the induction of CD4+T cells. These T-cells
secrete cytokines that lead to the production of IgE antibodies by the
plasma cells.
 Once again, the IgE molecules bind to the FcERI receptor present on
the mast cells and basophils which in turn causes vasodilation,
increased vascular permeability and Vascular spasm (Yalew ST,
2020).

Page | 43
Page | 44
Components of type-I hypersensitivity reactions
a) Allergens
Von Pirquet was the first person to use the term allergen to represent all
the foreign substances that are capable of inducing immune responses. An
allergen is any substance that induces immediate hypersensitivity (Ajoy Paul,
2016).
b) Reagen
Reagen or reagenic antibodies are those antibodies found in the serum and
skin of the allergically hypersensitive person but are present in low fractions
in normal individuals. In Type-I reactions, IgE acts as a reagin. These reagins
are also known as homocytotropic antibodies or Prausnitz-Kustner antibodies
as K Prausnitz and H. Kustner worked on it in 1921 (Ajoy Paul, 2016).
c) Mast cells, basophils and eosinophils
d) Mediators of anaphylaxis
The preformed contents of mast cells and basophils act as the primary
mediators in the anaphylactic reactions. These are as follows:
Histamines
Histamines when released into the skin stimulate sensory nerves
producing burning and itching sensations. It causes vasodilation and
hyperemia by an axon reflex and edema by increasing capillary permeability.
It also induces smooth muscle contractions in diverse tissues and organs.
Serotonin
It causes smooth muscle contraction, increased capillary permeability,
and vasoconstriction.
Chemotactic factors
The eosinophil chemotactic factors of anaphylaxis (ECF-A) contribute to
the eosinophilia accompanying many hypersensitivity states.
Enzymatic mediators
Enzymatic mediators such as proteases and hydrolases are also released
from mast cell granules.
The secondary mediators are newly formed upon stimulation by mast
cells, basophils and other leucocytes. These are:

Page | 45
Prostaglandins and leukotrienes
It produces slow, sustained contraction of smooth muscles hence is
termed as a slow-reacting substance of anaphylaxis (SRS-A). prostaglandins
also affect the secretion by mucous glands, platelet adhesion, permeability,
dilation of capillaries, and the pain threshold
Platelet-activating factor (PAF)
It causes aggregation of platelets and release of their vasoactive amines.
There are several other biologically active substances that can also act as the
mediators of anaphylaxis such as anaphylatoxins released by the complement
activation, and other kinins formed from plasma kininogens (Reba Kanungo,
2017).
Sub-types
a) Cutaneous or localized anaphylaxis
When a shocking dose of antigen in a small quantity is injected
intradermally in a sensitized host, a wheal and flare response occurs at the
administered site wherein the wheal is a pale central area of puffiness formed
due to edema which is surrounded by a flare caused by hyperemia and
subsequent erythema. Basically, localized anaphylaxis t is a type of
anaphylaxis that does not occur throughout the body instead is localized in the
affected region alone.
b) Systemic or generalized anaphylaxis
It is a form of immediate hypersensitivity (anaphylaxis) which occurs
when the mast cells and the basophils are induced to release the mediators
which can further elicit the immune response that is generalized throughout
the body.
c) Passive cutaneous anaphylaxis (PCA)
PCA is a test developed by Ovary in 1952 for in vivo detection of
antibodies. when a small volume of antibody is injected intradermally whereas
the antigen combined with dyes like Evans's blue etc., is injected intravenously
into a normal animal, after a period of 4-24 hours, immediate bluewing at the
site of intradermal injection happens due to vasodilation and increased
capillary permeability showing a wheal-and-flare reaction.
d) Acute anaphylaxis
Acute anaphylaxis is a severe allergic reaction that occurs when the rate
of release of the vasoactive molecule is greater than the body's ability to

Page | 46
respond to the rapid changes in its vascular system. If not administered on time
it may lead to the death of an individual. Hence, acute anaphylaxis is also
termed as anaphylactic shock.
The effect of type-I anaphylaxis may range from asymptomatic, minor
inconvenience to severe, and even fatal when left untreated.
2. Type II hypersensitivity reactions (Antibody-dependent cytotoxicity)
 Type II hypersensitivity reactions are a type of immediate
hypersensitivity reaction that involves antibody-mediated
destruction of cells. Hence, is also known as a cytotoxic reaction
(Yalew ST, 2020).
 These reactions involve the IgG antibodies and sometimes the
combination of IgG and IgM immunoglobulins with the antigenic
determinants on the cell surface leading to cytotoxicity or cytolytic
effects (Reba Kanungo, 2017).
 The main mediators in this type of hypersensitivity are IgM, IgG, and
complement. The cell damage is a direct result of the actions of the
antibodies and the complement system.
 Antibodies directed against antigens on the surface of nucleated cells
or the red blood cells will cause their lysis in the presence of
complement.
 If the immunoglobulins are not the ones to activate complement, then
the target cell may still be destroyed by phagocytosis or Antibody-
dependent cellular toxicity (ADCC). Thus, this type of
hypersensitivity leads to a completely destructive process.
 The best example of type II hypersensitivity is the destruction of
foreign red blood cells following an incompatible blood transfusion
(Ian R. Tizard, 1995).
Mechanism of Type-II hypersensitivity
 Type-II hypersensitive reactions are intermediate between the actual
hypersensitivity and autoimmunity.
 In this reaction, specific antibodies such as IgG or IgM binds to the
antigen present on the surface of the cells forming antigen-antibody
(Ag-Ab) complexes and destroying the cells via complement-
mediated cell lysis (Ajoy Paul, 2017).
 Complement mediated cell lysis occurs with the help of a group of
inactive lytic enzymes generally present in the blood.

Page | 47
 The Ag-Ab complexes formed can activate the lytic enzymes of the
complement system by three different pathways. These involve: the
classical pathway, alternate pathway and the lectin pathway
 The activated complement system on the cell surface carries out cell
lysis in a cascade of mechanisms (Yatew ST, 2020).
 When the antibodies are unable to destroy or neutralize the antigen,
it acts as a mediator and subjects the cells to antibody-dependent cell-
mediated cytotoxicity (ADCC) by cross-linking the target cell with
the cytotoxic cell which then carries out the lysis of the target cell
(Yatew ST, 2020) (Shyamasree Ghosh, 2017).
 In ADCC, the Ab binds to the Ag through Fab region due to which
the FC region which has a surface receptor on the cytotoxic cell is
free. As a result of this, the formed Ag-Ab complex, with the help of
the free FC region binds to the surface receptor of the cytotoxic cells
such as NK cells, macrophages, neutrophils, and monocytes thereby
cross-linking the target cell and the Cytotoxic cell.
 These cross-linkages activate the phagocytes and lead to an increased
rate of phagocytosis (Shyamasree Ghosh, 2017) (Yatew ST, 2020).

Page | 48
3. Type III hypersensitivity reactions (Immune complex-mediated
hypersensitivity)
 Type III hypersensitivity reaction (Immune Complex Mediate
Reaction) is an unusual immune response which is triggered by the
accumulation of soluble immune complex (aggregations of antigens,
IgG and IgM antibodies).
 Soluble immune complex form in the blood and when they are not
removing from the circulation they will be deposited in various
tissue, typically the skin, kidney and joints.
 The accumulation of these immune complexes activates an immune
response which is according to the Classical Complement Pathway.
Activation of complement cause the inflammatory cells, like
neutrophils and monocytes, to come together and releases lysosomal
enzymes along with free radicals at immune complexes site and
damage the tissue.
Mechanism of type III (Immune complex) hypersensitivity reaction
Step I: Immune complex formation: The antigens (endogenous or
exogenous) bind to antibodies and form circulating immune complexes
(CICs), (Norina Usman et al., 2021). The CICs will deposit on the basement
membrane of the glomerulus in the kidney. This antigen-antibody binding,
activate the Classical Complement Pathway, and this activation leads to the
formation of complement fragments(C3b) which damage the basement
membrane.
Step II: C3a and C5a fragments that acts as Chemotaxin will recruit the
neutrophils and macrophages to the site where CICs is deposited. These

Page | 49
neutrophils bind with C3b through its receptor and tries to engulf CICs and
through this process, the neutrophils discharge proteolytic enzymes and toxic
substances on the CICs deposition site and destroys the basement membrane.
(Samiksha S)
Pathophysiology
 The pathogenicity of Circulating immune complexes is partially
depends on the antigen-antibody ratio. If the antibody is more, the
immune complexes do not circulate and are insoluble, and are eaten
up by the macrophages of the lymph nodes and spleen.
 But, when the antigen is more, the accumulation of immune
complexes is much smaller and can pass through the filtration of
organs and convert the blood into other fluids such as urine and
synovial fluid.
 The symptoms of type III hypersensitivity develop according to the
site of deposition, i.e.; symptoms of glomerulonephritis (glomeruli),
arthritis (joints) and vasculitis (blood vessels).
Diseases of Type III hypersensitivity reactions
1) Serum sickness.
2) Post-streptococcal glomerulonephritis.
3) Systemic lupus erythematosus.
4) Hypersensitivity pneumonitis (farmer’s lungs).
5) Rheumatoid arthritis.
4. Type IV hypersensitivity reactions (Delayed type or cell-mediated
hypersensitivity)
Type IV hypersensitive reaction, also known as Delayed Type
hypersensitivity (DTH) or cell mediated hypersensitivity, is a reaction that
occur when the skin is in contact with some allergens (contact dermatitis). It
is induced by T cells that cause inflammatory reaction against antigens.
After exposure to antigen, a primary immune and inflammatory response
occurs which recruit the leucocytes (macrophages) to the site of infection, and
release cytokines that cause tissue damage. Antigens is engulfed, processed
and presented by macrophage, monocytes or dendritic cells to the T Cells,
which later become activated. (Khaled Marwa. et al., 2021). Based on the type
of T cell (CD4 T-helper type 1 and type 2 cells) that involve in the reaction, it
is subdivided into Type IVa, IVb, IVc, and IVd.

Page | 50
Mechanism
1) Specific antigen is recognized by type 1 helper (TH1) T effector cells,
which stimulated to release chemokines that attract macrophages to
the site and release cytokines that damage the tissue and result to
illness.
2) Macrophages were activated by IFN-γ and increase the release of
toxic substances, whereas endothelial cells are activated by INF-α
and INF-β and allow penetration that damage the tissue.
3) The reaction takes place from 48 to 72 hours after exposure to the
allergen, hence it is considered as delayed hypersensitivity
The classical example of type IV hypersensitivity reaction is Contact
dermatitis (poison ivy, chemicals and certain metals) and Tuberculin
(Montoux) Test which is develop in the form of erythema. (Jane E. Salmon,
et al., 2012) (Dr. Shyamasree Ghosh, 2017).
5. Type V hypersensitivity reactions (Stimulatory hypersensitivity)
 It is a modified form of Type-II hypersensitivity, wherein, non-
complement fixing antibodies bind to the surface receptors of the
target cell and stimulates the excessive secretion of cytotoxic
components which in turn can activate the phagocytes rather than
directly destroying the antigen (Reba Kanungo, 2017) (Anthony P
Weetman, 2001).
 It involves the production of antibodies against a specific hormone
receptor present on a hormone-producing cell.
 The best example of type-V hypersensitivity reaction is "Grave's
disease" which is caused by the binding of antibodies to some of the
thyroid cells at thyroid-stimulating hormone receptor (TSH-R) and
then stimulates the excessive secretion of thyroid hormone (Gary
Kaiser, 2021).
Mechanism of type-v hypersensitivity
 Type-V hypersensitivity occurs when the antibody that mimics
ligand binds to the receptors (TSH-R) and stimulates the cells to
produce excessive hormones.
 These ligands are usually the hormones.
 The antibody mimicking the ligand induces similar though not same
intracellular changes in the cells which then stimulates it.

Page | 51
  Due to the differences in the kinetics of the interaction between
antibodies and receptors, the intracellular signaling pathway may be
activated.
 The stimulatory effect which occurs due to the binding of antibody
mimicking ligand is not the same as the effect of a natural ligand
binding to its receptors (Anthony P Weetman, 2001) (Gary Kaiser,
2021).
Overview of all the types of hypersensitivity reactions

Laboratory diagnosis
Allergy testing is carried out for identification of an allergens capability
to stimulate immune system to produce an allergic reaction.
A. Skin test: Skin test can by performed to identify the allergens or
etiological organism. This can be done by below mentioned tests.
1) Skin prick test: It is also called scratch test. This test is usually used
to identify allergies to the pollen or dust mites. Especially, in adults
skin prick test is usually done on the forearm.
2) Intradermal test: Each foreign substance is injected Intra -dermally
to make a wheel, similar to tuberculin test. The concentration of
foreign substance is much higher at 1 to 500 or 1 to 1000. In this test,
two types of controls are used i.e., positive control and negative
control. If a skin prick test is being done at the same time, these
controls can be used.
3) Skin patch test: In this test a patch with the immune trigger is placed
on the skin, usually back, for 48 hours and according to the
observation, result is interpreted. It is used to find the skin allergy
(Katheryn Birch., et al., 2021).

Page | 52
 B. Blood test: Blood test is performed in order to count the levels of
immunoglobulin E (IgE) against specific foreign substance such as
foods, medications, latex venom. This test can confirm the diagnosis
of foreign substance disorder.
C. Diseases
1) Anaphylaxis
Anaphylaxis is medical response which can lead to an acute.
 It is an immunoglobulin mediated process.
 It is the most acute form of a susceptibility reaction.
 The mast cells instantly release a large amount of histamine.
 In acute cases, such as, intense bronchospasm, laryngeal edema,
hypertension can be seen (Wang KY., et al., 2019).
2) Allergic bronchial asthma
 It is an atopic disease, identified by bronchospasm.
 It is a chronic inflammatory disease.
1) Allergic rhinitis
 Unfavorable susceptible Rhinitis is another atopic sickness where
receptor and leukotrienes and answerable for rhinorrhea, wheezing
and nasal obstacle.
 Allergens are like those found in bronchial asthma. Nasal polyps
might be seen in persistent rhinitis. (Vandervoort R., et al.,2018).
2) Myasthenia gravis
 Gravis is an immune system issue made by antibodies post synaptic
acetocholine receptors that obstruct neuromuscular transmission.
 It is characterized by two folded visions, bilateral ptosis, conjunctiva
eye developments.
 Babies born to mothers with myasthenia gravis can have transient
muscle short coming because of pathogenic IgG antibodies that cross
the placenta.
3) Autoimmune Neutropenia
Immune system Neutroponeia might be available with bacteria and
parasitic contaminations, or it might happen alone or with immune system
sickness (Rheumatoid joint inflammation, immune system hepatitis), disease

Page | 53
and lymphoma. Bone marrow assessment is required in the event that
Neutroponeia is serious for related immune system issues an immune system
is an antibody panel is necessary (Justiz Vaillant A A, Zito PM et al., 2021).
4) Hemolytic disease of the fetus and the new born (Erythroblastosis
Fetalis)
The maternal resistant framework experiences an underlying sharpening
totb the fetal Rh +red platelets during birth when the placenta tears away. The
first child gets away from the sickness yet the mother, presently sharpened,
will be equipped for causing a hemolytic response against a second Rh+ fetus,
which creates Anemia, jaundice once the maternal IgG crosses the placenta.
(Leonard A., et al. 2019).
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