General introduction of the immune system Essay Example
General introduction of the immune system Essay Example

General introduction of the immune system Essay Example

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The human immune system is a complex and diverse system that is constantly changing. It plays a vital role in defending against various infections, including viruses, bacteria, and other harmful elements present in the air and food. These harmful elements are known as antigens, which stimulate the production of antibodies. Antigens are substances that can cause an immune response leading to the generation of antibodies that will interact with them.

The immune system depends on the intricate interaction of its components to defend against pathogens and react to their assaults on our body (Abbas AK and Lichtman, 2004; AH Janeway CA et al., 2001; Thomas J et al., 2006).

The innate immunity is the initial defense mechanism in the body, from birth onwards, to guard against infectious microorganisms. This form of immunity is nonspecific and does not have a memory component, offering immediate but limited prot


ection (Abbas AK and Lichtman, 2004).

The adaptive immunity, also referred to as acquired immunity, serves as the secondary line of defense in the body. It possesses antigenic specificity that enables it to detect even slight variations in antigens such as individual amino acids. Antibodies are capable of identifying these minor distinctions between two proteins.

The immune system has the capacity to generate a diverse array of recognition molecules, aiding in the identification of various structures on foreign antigens. Furthermore, the adaptive immune system possesses an exclusive attribute called immunological memory. This implies that upon encountering the same antigen again, a heightened immune response is activated. In typical situations, the immune system responds selectively to foreign antigens and can distinguish between self and non-self. This ability is crucial as an inappropriate reaction to sel

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molecules can have negative consequences (Roitt IM and Delves PJ., 2004; Janeway CA et al., 2001; Thomas J et al.).

The Innate Immune System: Components and Functions

The innate immune system includes external and internal defenses. The skin and mucous membranes serve as external barriers, offering unconditioned immunity by blocking the majority of pathogens from entering tissues. Moreover, the skin produces lactic acid and fatty acids to lower skin pH and act as bacteriostatic agents. Tear fluid not only serves a cleansing function for the eyes but also contains an enzyme called muramidase that specifically targets Gram-positive bacteria.

The respiratory tract and digestive tract both have protective mechanisms to prevent the entry of pathogens. In the respiratory tract, mucous secretion and ciliated epithelial tissue act as filters. Similarly, in the digestive tract, mucous secretion acts as a barrier to prevent the absorption and invasion of pathogens into cells. The stomach's acidic environment is responsible for killing microorganisms, while natural bacteria present in the lower intestine prevent pathogens from attaching (Abbas AK and Lichtman, 2004; Roitt IM and Delves PJ., 2004; Janeway CA et al).

, 2001; Thomas J et al., 2006). If a pathogen breaches the external innate defenses and invades the tissues, internal defense mechanisms provide protection. Internal, unconditioned immunity includes three general mechanisms: (1) physiologic barriers, (2) phagocytosis, and (3) inflammation. Physiologic barriers: supply rough environments to pathogens. These barriers include fluctuations of body temperature and O tension.

For example, when the body temperature of chickens is high, they are not susceptible to splenic fever. However, when their body temperature decreases, they become susceptible to this disease. Likewise, in the case of oxygen fluctuations, it has been observed

that anaerobic organisms like Clostridium perfringens (the causative agent of sphacelus) cannot grow in tissues with high oxygen concentration. Microorganisms can also activate a physiological barrier called the system of complement proteins, which leads to cell lysis. Similarly, in virally infected cells, two types of interferons (alpha and beta) are released. These interferons induce neighboring cells to produce chemicals that help suppress and prevent the spread of the viruses to other cells (Abbas AK and Lichtman., 2004; Roitt IM and Delves PJ.

According to Janeway CA et al. (2004) and Thomas J et al. (2001), the year mentioned here, other authors in 2006 also discussed this topic. The cellular innate immune response relies heavily on phagocytosis, a process in which specialized cells like macrophages and dendritic cells engulf and eliminate pathogens. Mobile cells such as monocytes, neutrophils, and eosinophils also play a role by traveling throughout the body via blood and lymph. Stuart LM (2005) explained that macrophages possess the ability to ingest and break down bacteria, as well as damaged or deceased host cells.

Macrophages have surface receptors that bind to sugars on bacteria, helping with the process of phagocytosis. During this process, macrophages release monokines such as interleukin-1 (IL-1), IL-6, and tumor necrosis factor-a (TNF-a). These substances play a crucial role in various inflammatory responses (Abbas AK and Lichtman., 2004; Roitt IM and Delves PJ., 2004; Janeway CA et al., 2001; Thomas J et al., 2006).

Neutrophils, also called polymorphonuclear neutrophilic leucocytes, are cells filled with granules that contain toxic digestive chemicals. They ingest micro-organisms for digestion and do not participate in presenting them to other immune cells. Neutrophils are the main source of defensins, which

are small peptides with a broad antimicrobial range. Defensins have non-specific cytotoxic activity against various normal and cancerous cells. Another group of granule-filled cells, called natural killer (NK) cells, do not engulf particles but contribute to the nonspecific defense against infected body cells and tumor cells (Abbas AK and Lichtman).

2004; Roitt IM and Delves PJ, 2004; Janeway CA et al., 2001; Thomas J et al., 2006). Inflammation occurs when phagocytosis is unable to control infection. It initiates through chemical mediators that induce the production of cytokines and chemokines at the site of infection. As a result, cells and plasma proteins are attracted to the area due to increased vascular permeability. This leads to common signs of inflammation including swelling, redness, pain, and heat (Li M et al.

In response to tissue damage, inflammation reactions release chemical mediators known as acute phase proteins. The main protein produced by liver cells due to tissue damage is C-reactive protein. C-reactive protein binds to the C-polysaccharide cell-wall constituent found on various bacteria and fungi. This binding activates the complement system, increasing clearance of the pathogen through complement-mediated lysis or a complement-mediated increase in phagocytosis (Abbas AK and Lichtman., 2004; Roitt IM and Delves PJ, 2001).

, 2004; Janeway CA et al., 2001; Thomas J et al., 2006). Histamine, another important mediator, is released by mast cells in response to tissue damage. It binds to receptors on nearby capillaries and venules, causing vasodilation and increased permeability. Mast cells play a crucial role in innate immunity against bacteria. Several studies have shown that the presence of mast cells is necessary for the host's survival after bacterial infection (Echtenacher et al., 1996; Malaviya et


Little peptides called kinins are a group of inflammatory mediators. They are typically found in an inactive form in blood plasma. When tissue damage occurs, these peptides are activated and cause vasodilation and increased permeability of capillaries (Abbas AK and Lichtman., 2004; Roitt IM and Delves PJ., 2004; Janeway CA et al., 2001; Thomas J et al., 1996a).

The adaptive immune system consists of two types: humoral immunity and cell-mediated immunity. It relies on the cooperation between lymph cells and antigen presenting cells to defend against various antigens.

2004; Roitt IM and Delves PJ, 2004; Janeway CA et al., 2001; Thomas J et al., 2006).

The Significance of Lymphocytes in the Immune System

Lymphocytes are an essential part of the immune system. They are generated in the bone marrow through haematopoiesis and then migrate through the blood and lymphatic systems to various lymphoid organs where they reside.
Lymphocytes play a crucial role in defending against harmful pathogens by creating cell-surface receptors that attach to antigens. B-Lymphocytes, also referred to as "the offspring cells produced in bone marrow or bursa," have a specific responsibility for humoral immunity. These cells can generate antigen-specific blood proteins known as antibodies or Igs.
B-Lymphocytes primarily identify extracellular antigens, including those on cell surfaces. When exposed to these antigens, B-Lymphocytes differentiate into plasma cells that release antibodies into circulation. This process effectively supports humoral immunity.

The immune response relies on antibodies, which have a crucial function of identifying foreign antigens and initiating a biological reaction that leads to the elimination of the antigen. In humans, B cells produce nine different antibody types: IgM, IgD, IgG1, IgG2, IgG3, IgG4, IgA1, IgA2, and

IgE. Among these types, IgM plays an important role during the initial interaction between the immune system and the antigen. Conversely, protein antigens primarily stimulate the production of IgG1 antibodies while polysaccharide antigens promote the development of IgG2 antibodies. Additionally? it is believed that respiratory viruses are particularly targeted by ?IgG3 antibodies.

The primary components of mucosal immunity are IgA and, to a lesser extent, IgM. These antibodies are generated and released directly at mucose membranes. IgE plays a significant role in immediate hypersensitivity reactions, defense against helminths, as well as allergy and asthma symptoms. Conversely, IgD is found in serum in minimal quantities and its function remains poorly understood ( Abbas AK and Lichtman., 2004; Roitt IM and Delves PJ).

The process of antigen presentation by B cells is supported by a unique cell type called follicular dendritic cell (FDC). FDCs possess membrane projections that enable them to present antigens to B lymph cells at certain stages of humoral immune responses. These specialized cells, known as antigen-presenting cells (APCs), connect the activities of both innate and adaptive immune systems, making them integral components of both systems. (Janeway CA et al., 2001; Thomas J et al., 2006; 2004)

Follicular dendritic cells (FDCs) are found in the lymphoid follicles of lymph nodes, spleen, and mucosal lymphoid tissues. They collaborate with activated B-cells and play a significant role in antigen presentation. FDCs capture antigens that are attached to antibodies or complement products and display these antigens on their surfaces. This allows B lymphocytes to strongly recognize and bind to the presented antigens, aiding in the selection of activated B cells. This process is essential for immune responses (Abbas AK

and Lichtman, 2004; Roitt IM and Delves PJ, 2004; Janeway CA et al).

According to Thomas J et al. in 2001 and 2006, T-Lymphocytes are derived from the thymus and can be divided into two subpopulations: T assistant (TH) cells and T cytotoxic (TC) cells. TH cells have CD4 on their surface, while TC cells have CD8. When exposed to antigens, TH cells release cytokines to stimulate the growth and specialization of T cells.

T cells have a variety of roles, such as activating B cells, macrophages, and other leukocytes. They also play a part in eliminating infected cells and assisting with immune suppression. Naive CD4 T helper cells are divided into four types: Th1, Th2, Th17, and Treg cells (Zhu J and Paul WE).

The Th1-Th2 paradigm is defined by the form of the cytokine response. Cytokines, which are proteins created by cells in the immune system, play a vital role in guiding immune responses and facilitating communication between different cell populations. These cytokines interact with specific receptors on cell surfaces, typically at low concentrations and short distances because they have a brief lifespan. Their main functions involve stimulating and regulating the immune system, including processes like cellular proliferation and chemotaxis. Cytokines are categorized into two types based on the T-helper cell type.

Th1 cells secrete interferon gamma (IFN) and tumor mortification factor alpha (TNF-a), while Th2 cells release interleukins including IL-4, IL-5, and IL-13. These cytokines serve as markers for macrophages and target B-cells, contributing to both cellular and humoral immune responses (Le Gros Z et al., 1990; Swain SL et al., 1990; Lombardi G et al., 2001; Daines SM., 2010).

T lymph cells have limited specificity for

antigens. They specifically recognize peptide antigens attached to host proteins that are encoded by genes in the major histocompatibility complex (MHC) and expressed on the surfaces of other cells. Hence, these T cells respond to cell surface associated but non-soluble antigens.

The MHC molecules are divided into two categories: MHC category I and MHC category II, each performing different functions. MHC category I molecules are involved in intracellular events such as viral infection, presence of bacteria within cells, or cellular transformation, and stimulate CD8+ T cells. MHC category I molecules consist of heavy chains and a constant light chain called beta-2 microglobulin.

The biogenesis of MHC category I molecules can be summarized in six steps: 1) acquisition of antigenic peptides, 2) labeling of antigenic peptides for destruction through ubiquitylation, 3) proteolysis, 4) delivery of peptides to the endoplasmic reticulum (ER), 5) binding of peptides to MHC category I molecules, and 6) presentation of peptide-MHC complexes on the cell surface.

The main role of MHC category II molecules is to interact with the extracellular environment and display antigens to CD4+ T cells, as stated by Jensen PE (2007). Both macrophages and dendritic cells are responsible for utilizing the antigen presentation pathways of MHC categories I and II. Dendritic cells function as antigen-presenting cells (APCs) by presenting microbial peptides to naive CD4+ and CD8+ T lymphocytes, thereby initiating adaptive immune responses towards protein antigens. These dendritic cells can be found in various organs, including epithelial and connective tissues, where they capture pathogens, break down their proteins into peptides, and exhibit them on specialized MHC category I molecules for peptide presentation.

The lymphoid organs have elongated cytoplasmic projections that enhance their surface

area, allowing them to effectively sample and absorb substances from the extracellular tissue environment through pinocytosis and phagocytosis. Dendritic cells also possess various surface receptors, including Toll-like receptors, which recognize pathogen-associated molecular patterns and transmit signals within the cell. Once activated, dendritic cells carry the antigenic peptides and travel through the lymph nodes, residing in the same areas where naive T lymphocytes continuously circulate. This concentration of antigen in recognizable form at specific locations greatly increases the chances of lymphocytes with antigen receptors encountering antigens (Vyas JM et al., 2008). B-lymphocytes and macrophages are responsible for capturing extracellular pathogens and presenting them to MHC class II molecules.

MHC class II Bachelor of Arts heterodimers antigen presentation relies on various components including a specialized type II transmembrane chaperone protein known as the invariant chain (Ii). This protein is responsible for ensuring stable assembly in the endoplasmic reticulum. The Ii contains a fragment that fits into the MHC class II peptide-binding channel, serving as an alternative peptide to stabilize the protein. Additionally, the Ii contains an endosomal sorting and retaining signal on the cytoplasmic domain (Watts C., 2004; Jensen PE et al.).

In 1999 and 1996, Cresswell P. published studies discussing the cleavage of the Ii protein by Cathepsin S, which leads to the release of the MHC class II ?? heterodimer from the Ii cytoplasmatic tail endosomal keeping signal. This process involves a series of events. The cleavage of Ii results in the formation of a short peptide called MHC class II-associated invariant-chain peptide (CLIP), which is protected from peptidase activity by binding to another peptide.

In the later phases, CLIP is replaced by other peptides in the endosomal

tract to operate the system. The catalyst-chaperone protein HLA-DM plays a crucial role in accelerating the rate of CLIP release and peptide exchange in MHCII compartments. HLA-DM is believed to modify the peptides presented to CD4+ T cells by catalyzing multiple rounds of peptide exchange, possibly favoring the most stable compounds. The pool of peptide antigens is derived from endosomal peptidases acting on both exogenous and endogenous proteins that enter the endosomal tract. If the cleft in the Class II MHC binds to one of the generated peptides, it becomes stable and is expressed on the surface. Otherwise, it is degraded by the peptidases in the endosome (Pieters J., 1997).

Immune system in Allergy

The term allergic reaction or serum illness was coined by Clemens von Pirquet in 1906. It describes an inappropriate immunological response of the acquired immune system after sensitisation by exogenic antigen (allergen), which is mostly proteins and triggers allergic responses (Rapaport HG., 1973). Initially, the antibody produced in response to allergen was called "allergin." This antibody is produced in tissues in response to antigen stimulation and specifically transports sensitivity reactions to different allergens both in vivo and in vitro.

Coca introduced the term "immediate allergy" to describe a specific allergic state. He named the substance that triggers the allergic response an "atopen," and the corresponding antibody a "reagin" or skin-sensitizing antibody. In animal experiments involving anaphylaxis, the antigen is referred to as an "anaphylactogen," and the antibody as an "anaphylactin" or anaphylactic antibody (Blumenthal MN., 1996; Gell PGH, Coombs RRA., 1963). The adverse immune reaction involving immunoglobulin E (IgE), which was discovered by Stanworth DR, is known as atopy. It is considered the

body's initial defense against invading pathogens and foreign particles (Stanworth DR).

According to the text, the term "allergen" is used to refer to any substance that is involved in immediate allergy and triggers reaginic or specific IgE antibodies. Allergens are defined in terms of the body's response to them during an allergic reaction. The immune response in atopy is a result of the interaction between the host and an allergen, as well as other environmental factors that modulate it. Some examples of these allergenic sources include house dust mites (HDM) (Haugaard L et al., 1993; McHugh SM et al., 1993).

, 1990; Wahn U et al., 1988), pollens from various grasses and trees (Amato GD et al., 1998; Boral D et al., 2004; Chew FT et al.).

Additionally, exposure to allergens from domestic pets danders which are dropping from the tegument and far has been documented by several studies (Sibanda EN., 2000; White JF and Bernstein DI., 2003; Kaneko Y et al., 2005; Hedlin G et al.).

, 1991 ; Valovirta E et al. , 1984 ; Van Metre Jr TE et al. , 1988 ; Varney VA et al. , 1997 ) . The allergen's allergenic response is determined by properties, environmental factors, and host factors including genetic susceptibility. Similarly, the term hypersensitivity describes the condition of individuals experiencing allergic reactions after exposure to allergenic elements.

These allergic reactions, also known as anaphylactic reactions, are classified as humoral immune responses that are triggered by the interaction between antigens and antibodies (Cohen SG., 2002).

Types of Hypersensitivity reactions

Immediate reactions, also referred to as early stage reactions, occur within minutes or the first hour after an allergic individual is exposed to the

allergen. In humans, these reactions are observed in conditions such as hay fever, perennial rhinitis, asthma, urticaria, and gastrointestinal allergies (Pepys J., 1953, Thomas J et al., 2006).

Allergic reactions can also be categorized based on the type of effector cells involved. For example, in immediate reactions, different immune effector molecules are induced by different antibody isotypes. IgE antibodies stimulate and enhance the degranulation of mast cells, which leads to the release of histamine and other molecules. Hypersensitivity reactions can also be triggered by IgE and IgM antibodies through the activation of the complement cascade reactions (Thomas J et al., 2006).

Delayed allergic reactions, also known as late stage reactions, occur after two or more hours of allergen exposure. The peak reactions are observed 6-9 hours later and typically resolve within 24-48 hours. In these reactions, activated T assistant (Th) cells or cytotoxic T cells (Tc) produce different cytokines which act as the effecter molecules (Pepys J., 1953; Thomas J et al., 2006).

The Gell and Coombs Classification of Hypersensitivity Reactions

Hypersensitivity reactions occur due to various immune mechanisms. In 1963, Gell and Coombs developed a classification system for hypersensitivity reactions, categorizing them into four categories (expanded to five by Rajan Television in 2003).

The allergic reactions in three categories are either entirely mediated by antibody or by the interaction of antigen with antibody, and they belong to the humoral immune responses. The four types are: IgE-mediated (type I), antibody-mediated (type II), and immune complex-mediated (type III). There is also a 4th type of hypersensitivity known as delayed-type hypersensitivity (DTH), or type IV, which depends on reactions within the cell-mediated subdivision. Each type involves distinct mechanisms, cells, and intermediary molecules,

as shown in figure 1 (Roitt IM and Delves PJ).

, 2004; Janeway CA et al., 2001; Thomas J et al., 2006).

IgE Mediated Type I Hypersensitivity Reactions:

The cause of IgE mediated allergic reaction is the sustained overrun of the Ig E.

The increase in IgE occurs because of the presence of various antigens in the environment, both indoors and outdoors. These antigens can be things like plant pollens, food particles, or other substances that enter the body through breathing or consumption. This leads to type I reactions, which involve different components or cells of the immune system (Poole JA., 2005). The immune system's decision to react to allergens depends on factors such as the type and amount of allergen, the behavior and type of antigen-presenting cells, substances that stimulate the innate immune response in the same environment, the tissue where exposure occurs, interactions between T and B lymph cells, costimulators, and genetic predisposition.

Antigen-presenting cells present processed allergens to T-helper lymph cells, which determines the development of different types of T-cell immunity. This determination is influenced by various cytokines, chemokines, costimulatory signals, and regulative T cells. IL-4 and IL-13, among other Th2-type cytokines, cause B cells to shift categories. This shift leads to the production of allergen-specific IgE antibodies that bind to receptors on mast cells and basophils. Upon re-exposure to the sensitized allergen, IgE Fc receptors on mast cells and basophils are activated, resulting in the release of biogenic mediators that are responsible for the symptoms of anaphylaxis. The discovery of regulative T cells has changed our understanding of immune regulation in the past decade. Peripheral T-cell tolerance is a key immune mechanism in the healthy response

to self antigens and non-infectious non-self antigens.

Naturally occurring CD4+, CD25+ regulatory T (Treg) cells and inducible populations of allergen-specific, IL-10-secreting Treg type 1 cells inhibit allergen-specific effector cells and play a central role in maintaining peripheral homeostasis and establishing controlled immune responses. On the other hand, Th17 cells are characterized by their expression of IL-17 (or IL-17A), IL-17F, IL-6, tumor necrosis factor-alpha, and IL-22, which induce local tissue inflammation by increasing the production of proinflammatory cytokines and chemokines (Roitt IM and Delves PJ., 2004; Janeway CA et al., 2001; Thomas J et al.).

, 2006 ) .

Functions of B-Cells

B lymph cells leave the bone marrow when they are matured and have IgM and IgD on their surfaces. The two steps are common to all Ig isotypes that are encoded downstream of IgM and IgD. The pre-B-cell phase is the one in which the first step occurs, in which individual heavy-chain variable ( VH ) , diversity ( D ) and joining ( JH ) coding DNAs randomly come together with defined joints to create a VH ( D ) JHA cassette that encodes an antigen-specific VHA domain. This VH ( D ) JHA cassette, which is situated just upstream of the constant ( C ) AµA coding DNAs, allows for construction of the Aµ -heavy-chain protein. The second step, known as class-switch recombination ( CSR ) , allows properly stimulated B cells to modify the isotype of the antibodies that they produce while maintaining the specificity of their antigen.

The process involves an irreversible exchange of the heavy chain cassettes of different isotypes (C) AAµ to create different heavy chains. This

important step is tightly regulated. The structural design of the CeA venue is shared with other CHA genes. Each heavy-chain isotype gene, excluding Cd, has a 5' intronic region that contains a switch region (S). This switch region consists of repeated tandem pentamers or a 49 base-pair sequence. Immediately upstream of the switch region is a section that encodes a short I exon and its enhancer. In individual CHA genes, such as IgE, the switch region (SeA) undergoes physical recombination with the Aµ switch region (SAµ) during CSR to form a DNA hybrid molecule Figure 1.1. (Geha RS et al., 2003).

SeA is excised downstream of VH ( D ) JHA and upstream of the CeA venue ( Fig. ) . The immediate connection of VH ( D ) JHA and Ce sequences, resulting from imprecise and heterogeneous SAµ-SeA ligation, creates a functional cistron that encodes IgE ( King CL et al. , 1990 ; Gauchat JF et al. , 1990 ; Jung S et al. , 1994 ).

Regulation of IgE CSR

The regulation of CSR in B-cells is accomplished through the collaboration of specific signals from cytokines and cell surface receptors. The cytokines interleukin-4 (IL-4) and IL-13, along with the tumour-necrosis factor receptor (TNFR) superfamiliy member A CD40, are involved in this process. Figure 1.2 illustrates how dendritic cells consume allergens, enabling the presentation of antigenic determiners to T cells.

Stimulating specific CD4+A T cells results in the production of interleukin-4 ( IL-4 ) and increased expression of CD40 ligand ( CD40L ) by T cells. Stimulating CD40 on allergen-specific B cells upregulates the expression of co-stimulatory molecules CD80 and CD86, facilitating

enhanced T-cell expression of CD40L and improved stimulation of B cells via IL-4 initiation. Additionally, CD40-mediated stimulation of B cells synergizes with IL-4-receptor ( IL-4R ) signals to enhance the transcription of C e germline transcripts ( C e GLTs ) and activation-induced cytidine deaminase ( AID ), rearrange the IgE genomic locus, and produce IgE antibodies.

Pollen Allergens in Allergic Diseases

Pollen from various tree species is a significant source of allergic reactions.

They can cause an allergic reaction mediated by IgE antibodies in seconds because pollen allergens are proteins or glycoproteins that dissolve in water. Because they can dissolve, they can easily pass through the mucous membrane of the upper and lower respiratory tract. At least two mechanisms expel the allergenic components of pollen from the cytoplasm. In isosmotic conditions, allergens quickly come into contact with accessible mucous membrane surfaces like the conjunctiva and nose, causing immediate allergic symptoms like allergic rhinitis. In a hypotonic environment, pollens quickly absorb water, expelling inhalable substances containing allergens that can reach the lower airways and trigger asthma (Suphioglu C., 1998). Olive pollen (Olea europaea) is the main cause of allergic respiratory diseases in the Mediterranean basin and some parts of North America (Bousquet J et al.).

, 1985; Wheeler AW., 1992). Allergic respiratory reactions globally occur due to pollens of Cypress species (Bass D et al., 1991; Caballero T et al.

, 1996; Panzani R et al., 1986; Mari et al., 1997; Midoro-Horiuti T et al., 1992; Orbman D., 1945; Yoo TJ et al.

In addition to being found in Japan and India, mugwort is also found throughout Europe, North America, and parts of Asia. Mugwort pollen can cause allergic reactions such

as hay fever. In India, important allergenic pollen comes from various trees and herbs including Prosopis juliflora, Ricinus communis, Morus, Mallotus, Alnus, Querecus, Cedrus, Argemone, Amaranthus, Chenopodium, Holoptelea, Brassica, Cocos, Cannabis, Parthenium, and Cassia.

, 2003) . It has also b

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