updated info. regarding role of interleukins in immunity against helminths.

3. Immunity relatively inefficient
Helminths are much adapted
Most helminths extracellular & too large for
phagocytosis
Growth is not exponential
Usually mild infections
No division inside host
Do not pose imminent threat
Over-dispersion.
Immunity relatively inefficient
Helminths are much adapted
Most helminths extracellular & too large for
phagocytosis
Growth is not exponential
Usually mild infections
No division inside host
Do not pose imminent threat
Over-dispersion.

5. 1.Host:
AGE
SEX
Genetic makeup –
HbA to HbB : More superior in resistance to H.contortus and O.ostertagii
Enhanced resistance to Cooperia oncophora in Zebu as compared to European cattle
Fasciola gigantica resistance in Indonesian thin tailed sheep (Hansen et al,1999)
Greater production of Th2-like cytokines (IL-4, IL-5, IL-13) in resistant breeds to
Haemonchus contortus (Sallé et al 2014)
2.Parasite:
Presence of adult worm delays larval development if a new infection takes place
as in E. granulosus in sheep and T saginata in cattle
Interspecific competition between helminths for nutrient and habitat

6. Humoral:
Usually IgE mediated
Cell mediated
 Immunity can be transferred to naïve animals by transfer of lymphoid
cells of infected animals and infected animals show DTH in Trichinella
spiralis (Wakelin, 1978)
 Immunity can be transferred to naïve animals by both lymphocytes and
serum in Trichostrongylus colubriformes
(J. K. Dineen and B. M. Wagland …1996)
 Immunity can be transferred to syngenic sheep by transfer of
lymphocytes in Haemonchus contortus. (Smith WD et al 1984)

7. *Dominance of Th1 or Th2 depends on :
Antigen presenting cell type
Co-stimulatory molecules
Cytokines
Nature and dose of parasite antigen
*Dominance of Th1 or Th2 depends on :
Antigen presenting cell type
Co-stimulatory molecules
Cytokines
Nature and dose of parasite antigen

10. Type 1 immunity

11. Usually found in early stages of helminth infection and
larval migration.
Few examples are:
Dead cysts of Taenia solium (E. Sciutto et al, 2000)
Peri-oval granuloma formation in Schistosoma mansoni
(E. J. Pearce et
al….1991)
Th1-like responses might act on migrating larvae of Fasciola spp
through the liver parenchyma (E Moreau et al …..2010)
Usually found in early stages of helminth infection and
larval migration.
Few examples are:
Dead cysts of Taenia solium (E. Sciutto et al, 2000)
Peri-oval granuloma formation in Schistosoma mansoni
(E. J. Pearce et
al….1991)
Th1-like responses might act on migrating larvae of Fasciola spp
through the liver parenchyma (E Moreau et al …..2010)

12. Journal of Neuroimmunology
Volume 127, Issues 1–2, June 2002

13. The Journal of Experimental Medicine " Volume 173 January 1991

14. Journal of Biomedicine and Biotechnology (2010)

15. Highly complex multicellular, multifactorial system
Refers to combined immune response, which includes both innate
and adaptive components.
Regulated by Th2 cells
Cytokines IL-4,IL-5,IL-9,IL-13.
Characterized by:
Highly complex multicellular, multifactorial system
Refers to combined immune response, which includes both innate
and adaptive components.
Regulated by Th2 cells
Cytokines IL-4,IL-5,IL-9,IL-13.
Characterized by:
B cell proliferation
Antibody production
Class switching
Eosinophilia and Mastocytosis

17. IL-33
TSLP
IL-25

20.  Source:
 Secreted by epithelial cells and other cell types (Th2
and mast cells)
 Functions:
 IL-25 induces the production of other cytokines,
including IL-4, IL-5 and IL-13 in multiple tissues,
which stimulate the expansion of Eosinophils

21. All three alarmins promote Th2 responses through their
ability to induce Th2 cytokine production from ILC2s.
(Natural helper cells, Nuocytes )
ILC2s like Th2 cells can produce IL-5, IL-9 and IL-13.

22. . Nat Rev Immunol 2011;11:375–88.

23. .

26. Source:
 Th2 cells
Mast cells
 Eosinophils
NK cells
Functions:
 Key role in the differentiation, maturation, and survival of
eosinophils derived from bone marrow precursors.
IL-5 has been shown to act on mast cell and basophil to
release vasoactive mediators
Source:
 Th2 cells
Mast cells
 Eosinophils
NK cells
Functions:
 Key role in the differentiation, maturation, and survival of
eosinophils derived from bone marrow precursors.
IL-5 has been shown to act on mast cell and basophil to
release vasoactive mediators

29. The Journal of
Immunology
March 15, 2011

30. *Sources:
*Primarily produced by Monocytes
*To a lesser extent by:
Type 2 T helper cells (TH2),
 Mast cells
Treg cells
*Sources:
*Primarily produced by Monocytes
*To a lesser extent by:
Type 2 T helper cells (TH2),
 Mast cells
Treg cells

33.  Specifically defined macrophages that respond to
signalling through the IL-4R alpha.
Have Receptors for both IL-4 and IL-13 and their receptors
share the common IL-4R chain, which is central to most
type 2 effector responses
IL-4 strongly induces a non-inflammatory response from
AAM..
 Specifically defined macrophages that respond to
signalling through the IL-4R alpha.
Have Receptors for both IL-4 and IL-13 and their receptors
share the common IL-4R chain, which is central to most
type 2 effector responses
IL-4 strongly induces a non-inflammatory response from
AAM..

35. Arginase .
Arginase suppresses the NO mediated anti-microbial pathways of
classically activated macrophages.
RELM-α ::
Stimulation of collagen production in myofibroblasts
(providing a potential link between alternatively activated
macrophages, fibrosis, and tissue repair
RELM β :
Intestinal goblet cells up regulate and secrete RELM-β under
the control of IL-13 signalling through the IL-4 receptor.
Arginase .
Arginase suppresses the NO mediated anti-microbial pathways of
classically activated macrophages.
RELM-α ::
Stimulation of collagen production in myofibroblasts
(providing a potential link between alternatively activated
macrophages, fibrosis, and tissue repair
RELM β :
Intestinal goblet cells up regulate and secrete RELM-β under
the control of IL-13 signalling through the IL-4 receptor.

36. .
*The factors involved in the
activation of eosinophils
*Granulocyte-macrophage
colony-stimulating factor (GM-
CSF)
*EAF ; Eosinophil Activating
Factor
*PAF ; Platelet-Activation
Factor
Text book of veterinary immunology 9th
edition Ian R Tizzard

37. Cellular and Molecular Immunology 7th
edition

38. .
Text book of veterinary immunology 9th
edition Ian R Tizzard
EPO: oxidants and NO
ECP,ENT: Ribonucleases

39. Potent inflammatory cells that are distributed throughout mucosal
barrier tissues
Mucosal mast cell proteinases are secreted in serum and local
intestinal secretions during expulsion of GI nematodes
(Woodbury et al., 1984)
MCs play an important role as late-stage effectors
Mastocytosis controlled by IL3, IL9 and other stem cell factors
Potent inflammatory cells that are distributed throughout mucosal
barrier tissues
Mucosal mast cell proteinases are secreted in serum and local
intestinal secretions during expulsion of GI nematodes
(Woodbury et al., 1984)
MCs play an important role as late-stage effectors
Mastocytosis controlled by IL3, IL9 and other stem cell factors

40. .
Mast cells
Histamine 5HT Proteinases
Prostaglandin
s
Leucotrienes
Increased mucosal permeability/SM contraction

43. Immunity against helminths differs from bacterial and viral
immunity
Helminths typically induce Type 2 immune response through the
production of cytokines IL-4,IL-5,IL-9,IL-10, and IL-13.
Th1 responses are found only in early stages like larval migration.
Type 2 response is non inflammatory response.
Interleukins act on both innate effector cells and adaptive effector
cells.
AAM plays main role in tissue repair through IL-4 and IL-13.
Eosinophils play role in parasite killing
Interleukins hence lead parasite killing, expulsion and tissue
repair
Immunity against helminths differs from bacterial and viral
immunity
Helminths typically induce Type 2 immune response through the
production of cytokines IL-4,IL-5,IL-9,IL-10, and IL-13.
Th1 responses are found only in early stages like larval migration.
Type 2 response is non inflammatory response.
Interleukins act on both innate effector cells and adaptive effector
cells.
AAM plays main role in tissue repair through IL-4 and IL-13.
Eosinophils play role in parasite killing
Interleukins hence lead parasite killing, expulsion and tissue
repair

44. [1] Immunology of Parasitic Helminth Infections :Andrew S. MacDonald, MariaIlma Araujo, and
Edward J. Pearce INFECTION AND IMMUNITY, Feb. 2002, p. 427–433
[2] Protective immune mechanisms in helminth infection Robert M. Anthony, Laura I. Rutitzky, Joseph F.
Urban Jr, Miguel J. Stadecker‡, and William C. Gause|| Eur J Immunol. 2003 Sep;33(9):2382-90
[3] Anthony RM, Rutitzky LI, Urban JF, Stadecker MJ, Gause WC. Protective immune mechanisms in
helminth infection. Nat Rev Immunol 2007;7:975–87.
[4] Licona-Limón P, Kim LK, Palm NW, Flavell RA. TH2, allergy and group 2 innate lymphoid cells.
Nat Immunol 2013;14:536–42.
[5] Saenz SA, Taylor BC, Artis D. Welcome to the neighbourhood: epithelial cell derived cytokines
license innate and adaptive immune responses at mucosal sites. Immunol Rev 2008;226:172–90.
[6] Gause WC, Wynn TA, Allen JE. Type 2 immunity and wound healing: evolutionary refinement of
adaptive immunity by helminths. Nat Rev Immunol 2013;13:607–14.
(7) Allen JE, Maizels RM. Diversity and dialogue in immunity to helminths. Nat Rev Immunol
2011;11:375–88.
(8) Tom N. McNeilly,and Alasdair J. Nisbet Immune modulation by helminth parasites of ruminants:
implications for vaccine development and host immune competence Tom N. McNeilly, and Alasdair J.
Nisbet Parasite 2014, 21, 51
(9) Ian R Tizzard Textbook of veterinary immunology 9th
edition
[1] Immunology of Parasitic Helminth Infections :Andrew S. MacDonald, MariaIlma Araujo, and
Edward J. Pearce INFECTION AND IMMUNITY, Feb. 2002, p. 427–433
[2] Protective immune mechanisms in helminth infection Robert M. Anthony, Laura I. Rutitzky, Joseph F.
Urban Jr, Miguel J. Stadecker‡, and William C. Gause|| Eur J Immunol. 2003 Sep;33(9):2382-90
[3] Anthony RM, Rutitzky LI, Urban JF, Stadecker MJ, Gause WC. Protective immune mechanisms in
helminth infection. Nat Rev Immunol 2007;7:975–87.
[4] Licona-Limón P, Kim LK, Palm NW, Flavell RA. TH2, allergy and group 2 innate lymphoid cells.
Nat Immunol 2013;14:536–42.
[5] Saenz SA, Taylor BC, Artis D. Welcome to the neighbourhood: epithelial cell derived cytokines
license innate and adaptive immune responses at mucosal sites. Immunol Rev 2008;226:172–90.
[6] Gause WC, Wynn TA, Allen JE. Type 2 immunity and wound healing: evolutionary refinement of
adaptive immunity by helminths. Nat Rev Immunol 2013;13:607–14.
(7) Allen JE, Maizels RM. Diversity and dialogue in immunity to helminths. Nat Rev Immunol
2011;11:375–88.
(8) Tom N. McNeilly,and Alasdair J. Nisbet Immune modulation by helminth parasites of ruminants:
implications for vaccine development and host immune competence Tom N. McNeilly, and Alasdair J.
Nisbet Parasite 2014, 21, 51
(9) Ian R Tizzard Textbook of veterinary immunology 9th
edition