**1.1 Characteristics: morphological, physiological, origin, immunological regulation, and distribution of eosinophil**

Eosinophils are leukocytes (white cells) found in the peripheral blood, hematopoietic, lymphatic organs, the bone marrow, spleen, and thymus, and can migrate to connective tissues and digestive tract; they are part of the group of leukocytes called granulocytes, along with basophils and neutrophils. They were described

by P. Ehrlich in 1879 calling them eosinophils because their acidic granules in the cytoplasm were stained by their affinity dye aniline-eosin giving them the form of red-orange ammunition observed by optical microscopy: They are rounded cells from 8 to 15 μm in diameter, with a bilobed core with a fine nuclear bridge joining both lobes [1].

Identification and quantification.

Methodology: Manual count in Neubauer chamber and automatic hematology analyzer using impedance and colorimetry and flow cytometry CD16 (FcƳRIII-CD16). Under normal conditions peripheral blood eosinophils represent 1–5% of total leukocytes, with an upper limit of 0.4 × 109 L,, the absolute eosinophilic count (AEC) of 350–500/mm3 and in children is greater than 0.75 × 109 L, increasing the number of eosinophils (eosinophilia) to more than 3–5 times which is indicative of an activity of infectious, parasitic, allergic, and eosinophilic and hypereosinophilic disorders [1–5].

They originate in the bone marrow, by a process of maturation and differentiation that lasts approximately 8 days (hematopoiesis) from a pluripotential precursor cell (stem cell) differentiating itself as myeloid granulocytic line, under the influence of IL-3, IL-4 - granulocytic colony stimulation factor (GM-CSF) of eotaxin; evolving toward a mixed eosinophil-basophilic precursor and then differentiating toward eosinophils by action of IL-3, GM-CSF, and especially IL-5, they have a survival of 6–12 hours before moving to tissues where they remain between 2 and 5 days; once there is a stimulus, they respond by exercising their multiple functions regulated by T lymphocytes (**Figure 1**) [1, 2, 6].

The text begins with: Its main functions are the defense against parasites, helminths, nematodes, participate in allergic responses, inflammatory processes, restoration, and tissue repair; since they have specific chemotactic receptors on their membrane, eotaxin, cytokines (IL-3 -IL-5 and GM-CSF), eosinophil chemotactic factor of anaphylaxis (ECF-A); and nonspecific such as f MLP (from the wall of bacteria), complement activation products (C3a, C5a, C6, and C7), plateletactivating factor (PAF), leukotrienes (LTB 4 and LTD 4), histamine and IL-8. Diapedesis is mainly performed by integrins to adhere to the vascular endothelium

#### **Figure 1.**

*Scheme representing hematopoiesis, origin of eosinophil and its main functions associated with eosinophilic disorders. Molecules expressed on its surface (FcεRI-CD23-IgE). CCR4, CD88,H4R. Adhesion molecules: CD11b, CD11c, CD62L, and chemokines that attract eosinophils from blood to tissues [3, 7].*

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*Eosinophilic Disorders: Extrinsic and Intrinsic Immune Response, New Diagnostic Perspectives…*

(e.g., LFA-1-ICAM-1, the VLA-VCAM-1) and other multiple antibody receptors: IgA (Fc α R1-CD89), (FcεRIII-CD23-IgE), (FcƳεRI-degranulation), (FcƳRI-CD64-IgG1, IgG3 respiratory burst induction of microbial death), (FcƳA-CD32-Ig G1-degranulation), (FcƳRIIB-CD32-IgG1-No Phagocytosis, inhibition of cellular

Granular content: Eosinophil mature contains in its cytoplasm primary granules rich in phospholipase A, rich in crystalline proteins of Charcot-Leyden-specific secondary granules containing the major or main basic protein (MBP), the eosinophilic peroxidase (EPO), eosinophilic protein (ECP)), and eosinophil-derived neurotoxin (EDN) that also appears in basophils and neutrophils; its response capacity is less than 1 hour, small granules containing arylsulfatase B and acid phosphatase and five lipid bodies main source of arachidonic acid, can be presenting cells, proliferation of T lymphocytes and basophils are capable of deliberating more than 35 cytokines,

The severity of eosinophilia has been arbitrarily divided into mild (AEC from

The classification of eosinophilic diseases was revised in 2008 and reaffirmed in 2016. In 2017 its diagnosis, risk stratification (prognosis), and management (treat-

Eosinophilic diseases can be classified in two types: primary, intrinsic hematology due to clonal disorders, and secondary, extrinsic or reactive disorders to an external cause that cause damage to different organs. Primary eosinophilias or clonal disorders can be diagnosed by studying the blood and bone marrow by the following methods: standard cytogenetics, molecular biology with monoclonal antibodies, flow cytometry, in situ hybridization, and evaluation of T cell clonality. The major category of primary diseases corresponds to myeloid/lymphoid neoplasms with eosinophilia and rearrangements PDGFRA, PDGFRB, or FGR1; with PCMiJAK2 and MPN, a subtype of chronic eosinophilic leukemia or not specified by CEL-NOS, there is another lymphoid-eosinophilic variant of aberrant T cell clone. The modern definition of hypereosinophilic syndrome (HES) is a vestige of the historical criteria outlined by Chusid and colleagues in 1975: The absolute eosinophil

The Working Conference on Eosinophil Disorders and Syndromes proposed a new terminology for eosinophilic syndromes. Hypereosinophilia (HE) for persis-

To have to a better understanding of the pathogenetic aspects of eosinophilia, other classifications of eosinophilic diseases were generated according to the site of eosinophilic infiltration associated with organ damage and dysfunction. The primary cause of eosinophilia located within the eosinophils (and/or eosinophil precursors) themselves or in other cells, similar to allergic diseases, can be divided in IgE-mediated (extrinsic) and non-IgE-mediated (intrinsic) diseases; the terms extrinsic and intrinsic eosinophilic disorders indicate whether the primary cause of

into a hereditary (familiar) variant (HEfa); HE of undetermined significance (HEus), primary (clonal-neoplastic), HE produced by clonal/neoplastic eosinophils (HEn), and secondary (reactive) (HEr) can be considered a provisional diagnosis

until a primary or secondary cause of eosinophilia is ascertained [12].

eosinophilia is inside or outside the eosinophil lineage [11].

ment) proposed by the World Health Organization were covered [10].

), moderate (AEC 1500–5000/mm3

for more than 6 months, and tissue damage is present [10, 11].

) in turn, HE subtypes were divided

), and

*DOI: http://dx.doi.org/10.5772/intechopen.89229*

chemokines, and growth factors (**Figure 1**) [5, 9].

).

tent and marked eosinophilia (AEC >1500/mm3

activity) (**Figure 1**) [2, 6, 8].

**2. Diseases and classification**

severe (AEC >5000/mm3

count is >1500/mm3

the upper limit of normal to 1500/mm3

*Eosinophilic Disorders: Extrinsic and Intrinsic Immune Response, New Diagnostic Perspectives… DOI: http://dx.doi.org/10.5772/intechopen.89229*

(e.g., LFA-1-ICAM-1, the VLA-VCAM-1) and other multiple antibody receptors: IgA (Fc α R1-CD89), (FcεRIII-CD23-IgE), (FcƳεRI-degranulation), (FcƳRI-CD64-IgG1, IgG3 respiratory burst induction of microbial death), (FcƳA-CD32-Ig G1-degranulation), (FcƳRIIB-CD32-IgG1-No Phagocytosis, inhibition of cellular activity) (**Figure 1**) [2, 6, 8].

Granular content: Eosinophil mature contains in its cytoplasm primary granules rich in phospholipase A, rich in crystalline proteins of Charcot-Leyden-specific secondary granules containing the major or main basic protein (MBP), the eosinophilic peroxidase (EPO), eosinophilic protein (ECP)), and eosinophil-derived neurotoxin (EDN) that also appears in basophils and neutrophils; its response capacity is less than 1 hour, small granules containing arylsulfatase B and acid phosphatase and five lipid bodies main source of arachidonic acid, can be presenting cells, proliferation of T lymphocytes and basophils are capable of deliberating more than 35 cytokines, chemokines, and growth factors (**Figure 1**) [5, 9].
