Innate Immunity Antibodies

Eosinophils

Characterization, markers and antibodies

Eosinophils are granulocytes which have the characteristic large cytoplasmic granules and bi-lobed nucleus. They can be found not only in the bone marrow and blood stream but also in tissues including; the thymus, lower gastrointestinal tract, ovary, uterus, spleen and lymph nodes (Uhm et al. 2012). Eosinophils make up approximately 1% of circulating leucocytes, rising to around 3-5% when activated. Eosinophils are short lived in peripheral blood lasting for up to 12 hours, however they can remain in tissues up to 12 days when in a steady unstimulated state.

Eosinophils are derived from CD34+ progenitor cells that are located either in the bone marrow or in other tissue such as the lung (Rosenberg et al. 2013). The exact process of eosinophil development is complex and not fully understood; it is thought to involve many different stages of intermediate progenitor cells.  Differentiation involves transcription factors such as CCA AT/enhancer protein, GATA1 and PU.1, and is stimulated by IL-3, IL-5, GM-CSF and other growth factors (Rosenberg et al. 2013, Uhm et al. 2012). There are differences between the development of human and mice eosinophils as in mice they arise from granulocyte-macrophage progenitors in the bone marrow (Rosenberg et al. 2013). Once eosinophils have matured and left the bone marrow they do not appear to proliferate (Uhm et al. 2012) but circulate in the blood and migrate to tissues at sites of infection/inflammation. It is here that they are then activated by effector molecules including IL-3, IL-5 and GM-CSF.

Eosinophils play an important and varied role in the immune response, aided by the fact that they can localize to tissues as well as the blood stream and they can activate both the innate and adaptive immune response. In the latter eosinophils have been shown to stimulate T cells and aid the long term survival of plasma cells (due to the production of the plasma cell survival factor APRIL) in the bone marrow and the lamina propria (Berek 2016 and Uhm et al. 2012). The role is achieved by the release/production of many different effectors molecules;

  • Cationic granules (released by degranulation) (Uhm et al. 2012)
  • Cytokines e.g. IL-2, IL-4, IL-5, IL-6, TNF-α and GM-CSF (Hogan et al. 2008)
  • Growth factors e.g. TGF-β, VEGF and PDGF (Kato et al. 2005)
  • Enzymes
  • Lipid mediators e.g. eicosanoids (Bandeira-Melo et al. 2002)

Therefore they have a role in fighting viral and parasitic infections. It is the accumulation of all these factors that means eosinophils have a major role in inflammation and allergic reactions, having been linked to the pathogenesis of Asthma (Uhm et al. 2012). Eosinophilia is a disease where there is a high level of eosinophils in the blood, usually as a result of a parasitic infection, allergic or autoimmune disease such as Asthma.

A number of different markers can be used to identify eosinophils. To view antibodies available to these markers simply click on the marker.

Human Markers

Mice Markers

CD9

CD9

CD11b

CD11b

CD11c

CD23

CD23

CD24

CD24

CD32

CD32

CD35

CD43

CD43

CD45

CD64

CD49d

CD126

CD62L

CD170

CD88

CD193

CD183

CD218α

CD193

CD294

CD198

Gr-1

CD294

Siglec-F

FcƐRIII

 

H4R

 

Siglec-8

 


References
  • Bandeira-Melo C et al. (2002). The cellular biology of eosinophil eicosanoid formation and function. J Allergy Clin Immunol. 109, 393-400.
  • Berek C. (2016). Eosinophils: importnant players in humoral immunity. Clin Exp Immunol. 183, 57-64.
  • Hogan SP et al. (2008). Eosinophils: biological properties and role in health and disease. Clin Exp Allergy. 38, 709-750.
  • Kato Y et al. (2005). Leukotriene D4 induces production of transforming growth factor-beta1 by eosinophils. Int Arch Allergy Immunol. 137, 17-20.
  • Rosenberg HF et al. (2013). Eosinophils: changing perspectives in health and disease. Nat Rev Immunol. 13, 9-22.
  • Uhm TG et al. (2012). Eosinophil development, regulation and eosinophil-specific genes, and role of eosinophils in the pathogenesis of Asthma. Allergy Asthma Immunol Res. 4, 68-79.