- Email: [email protected]
From parasites to allergy: the role of IgE receptors on inflammatory cells
Symposiam (I) / Parasitology
InrenzationaI47
(Suppl.) (1998) 63-70
6.5
I-l. Allergy and Parasitic Diseases s-11-1
FROM PARASITES TO ALLERGY: THE ROLE OF I@ RECEPTORS
ON INFUMhJATORY
POLARISATION OF THE IMMUNE RESPONSE TO A SCHISTOSOMF ANTIGEN BY A MITE ALLERGEN DER-P 1.
S-11-3
CELLS
Andre CAPRON Unit6 Inserm Ill67 - lnstitut Pasteur de Lille, FRANCE
C&Q&$*, Comoy E*, Pestel J**, Stewart GA***, Finkelman
High and low aflinity receptors for IgE have now been characterized at a molecular level on proir&mmatoty cell populations (macrophages, eosinophils, platelets) as well as on dendritic cells and Langerhans cells.
F****, Capron A*, Thyphronitis G*. *Unite INSERM 167, **Unit6 INSERM 416, Institut F&_i&atif de Recherche 17, Institut Pasteur de Lille, France, ***Department of Microbiology, University of Australia. Western ****Department of Medicine, University of Cincinnati, USA.
Evidence these cell immunity regulatory
A common property of many allergens and parasite antigens is their potential to generate type 2 cytokine responses, including specific IgE antibodies and eosinophilia. Jn order to understand this phenomenon, we have used immunization procedures with a well-characterized Schisrosoma mansoni antigen, Sm28-GST. Whereas immunization of mice with Sm2g-GST using CFA as adjuvant, induced a non-polarized immune response, a type 2 immune response was induced when alum was used. Coadministration of the major house dust mite allergen, Dwmatophagoides pteronyssinus (Der pl) together with SmZSGST is able to influence the immunological profiles induced by immunization with CFA. Introduction of Der pl in the CFA immunization protocol induced a decrease in anti-SmZB-GST lgG2a titers and reduced IFN-y mRNA expression, whereas the IL-4 OK IgG isotypic response was unaffected in the case of the alum protocol. The effect of Der pl is specific and dependent upon its protease activity. These results suggest that due to its protease activity, an allergen Der pl is able to modulate the immune response to a parasitic antigen, by influencing the balance between the antagonistic cytokines IL-4 and IFN-7. They illustrate the complexity of the immune response, specially in the context of multi-infected populations.
has now been obtained that IgE dependent activation of populations leads to the expression of effector functions in to hehninth parasites or to the release of inflammatory or molecules.
Similarities observed in antiparasite immunity and in allergic reactions will lead to some considerations regarding the role of IgE as an important signal of cell communication.
Reference
s-11-2
ROLE OF IL-3 AND STEM CELL FACTOR IN MUCOSAL MASTCYTOSIS
AND DEFENCE
AGAINST
S-II-J
: Comoy et al, J Immunol, 1998, 1602456-2462.
PROTECTION AGAINST TRICHINELLA SPIRALIS
INTESTINAL CONTROLLED BY ATOPY GENE IN MICE.
HELMINTHS
N&&y’, Kobayashi T, Abe T’, Lantz CS”‘, Galli SP”
lDepartmmt of Patssit&gy, Miyazaki Medical College, Miyazaki, l*De+tmert! of Pmasitology, AkJta Univ. School of Medicine, Akita, “‘Dqartmeat
Japan,
Departmen of Tropical Medicine, Jikei University School of Medicine.
Japan,
of Pathology, Beth Ismel Deacxmess Medic4 Center and Harvard
Tokyo. Japan.
Medical School, Boston USA
We previously reported that IgE responsiveness in mice is regulated &type specifically by a single autosomal gene not linked to H-2. The gene c~“Uols
Role of IL-3 and stem cell factor in nmasai agaimt intestinal hehninths was studied. wezc infeztcd eitha with S@~gr/oi&
mactcytosis and mucosal defencc
When “I& cellddicinrt
W/W” mice
rotti (S r) or S. Veneruelensis (S V),
expulsion of these parasites fmm the intestine was significantly delayed m-4 with that from normal littemmte +/+ mice. Delayed expulsion as well as defe&e i”testi”al mas( cell response in W/FV mice were normalized by bone marrow grafting.
Cmwu-sely, Sr-infcted ““de mice wae treated with murine U-3,
i”tcsti”al “ustocytosis was induced and the worms were expeled, so~esting
that
IL-3dcpcndcntly pmllfaated intestinal mast cells play a critical mle ir! expulsion of Slrongyloides spy.
7hi
concept was strengthened fmther by the fact that
expulsion of S v was delayed for 2 weeks in ILJ-knock defect was int&uc&
out mice. When IL-3-
into W/WVmice, S Y infection even persisted 0vQ 7 we=&.
These results suggest that both SCF and IL-3 are utilized i.n intestinal mast Cdl gmeration and mucosal defence agai”st intestinal parasites. Intestinal nustocytosis was i”doced by S Y infection in A/J and C58/J mice, of which bone “mmxv cells
capacity of IgE pmdwtior~ unrelated to antigens stimulated. Under this atopy gene,
strains of mice separated into IgE high and low responders. After T.spimlis infection. high respond.% (BALB/c. C3H, CDFl) produced larger amounts of lotal IgE and anti-T.spirohs IgE antibody than low responder(SJL). I@ dependencyof
protection to T.spiro/is was determined by comparison of the number of muscle larvae between IgEdeficient and IgE-producing conuol in each main. Selective IgE deficient mice were obtained by repealed injections of anti-IgEantibody. The IgE dependency of protection was found in IgE high responder suains but not in low responder strain. The effect of atopy gene orethe protection was confumed in backnoss
[(high-BALE/c x low-SJL)Fl x SJL] mice infected with T.sprralis. The
backcross mice segregated into IgE-high and low responders witi the ratio Of
I
I!
indicating a single gene. The number of muscle larvae recovered from IgE high
responders in backcross mice were signiiicanlly smaller than those of low
were non-m&tive to IL-3 in v&o due to a bra”& point nwlation in the IL-3Ra
responders. No significantly different number of muscle larvae was recoveredtram
gene. Sincz nmst cells could be induced from bone marrow cells of these mice by
both H-2 types of backcross mice, These results suggest that the alopy gene
co-presma
conuols protection to T.spirohs.
of IL-3 and SCF, S Y infection obviously stimulate in viva pmduc(ion
of these cytoki~~es. Our series of study indicate the inqortance of SCF and IL-3 in mast cell devdopment and parasite immunity
InrenzationaI47
(Suppl.) (1998) 63-70
6.5
I-l. Allergy and Parasitic Diseases s-11-1
FROM PARASITES TO ALLERGY: THE ROLE OF I@ RECEPTORS
ON INFUMhJATORY
POLARISATION OF THE IMMUNE RESPONSE TO A SCHISTOSOMF ANTIGEN BY A MITE ALLERGEN DER-P 1.
S-11-3
CELLS
Andre CAPRON Unit6 Inserm Ill67 - lnstitut Pasteur de Lille, FRANCE
C&Q&$*, Comoy E*, Pestel J**, Stewart GA***, Finkelman
High and low aflinity receptors for IgE have now been characterized at a molecular level on proir&mmatoty cell populations (macrophages, eosinophils, platelets) as well as on dendritic cells and Langerhans cells.
F****, Capron A*, Thyphronitis G*. *Unite INSERM 167, **Unit6 INSERM 416, Institut F&_i&atif de Recherche 17, Institut Pasteur de Lille, France, ***Department of Microbiology, University of Australia. Western ****Department of Medicine, University of Cincinnati, USA.
Evidence these cell immunity regulatory
A common property of many allergens and parasite antigens is their potential to generate type 2 cytokine responses, including specific IgE antibodies and eosinophilia. Jn order to understand this phenomenon, we have used immunization procedures with a well-characterized Schisrosoma mansoni antigen, Sm28-GST. Whereas immunization of mice with Sm2g-GST using CFA as adjuvant, induced a non-polarized immune response, a type 2 immune response was induced when alum was used. Coadministration of the major house dust mite allergen, Dwmatophagoides pteronyssinus (Der pl) together with SmZSGST is able to influence the immunological profiles induced by immunization with CFA. Introduction of Der pl in the CFA immunization protocol induced a decrease in anti-SmZB-GST lgG2a titers and reduced IFN-y mRNA expression, whereas the IL-4 OK IgG isotypic response was unaffected in the case of the alum protocol. The effect of Der pl is specific and dependent upon its protease activity. These results suggest that due to its protease activity, an allergen Der pl is able to modulate the immune response to a parasitic antigen, by influencing the balance between the antagonistic cytokines IL-4 and IFN-7. They illustrate the complexity of the immune response, specially in the context of multi-infected populations.
has now been obtained that IgE dependent activation of populations leads to the expression of effector functions in to hehninth parasites or to the release of inflammatory or molecules.
Similarities observed in antiparasite immunity and in allergic reactions will lead to some considerations regarding the role of IgE as an important signal of cell communication.
Reference
s-11-2
ROLE OF IL-3 AND STEM CELL FACTOR IN MUCOSAL MASTCYTOSIS
AND DEFENCE
AGAINST
S-II-J
: Comoy et al, J Immunol, 1998, 1602456-2462.
PROTECTION AGAINST TRICHINELLA SPIRALIS
INTESTINAL CONTROLLED BY ATOPY GENE IN MICE.
HELMINTHS
N&&y’, Kobayashi T, Abe T’, Lantz CS”‘, Galli SP”
lDepartmmt of Patssit&gy, Miyazaki Medical College, Miyazaki, l*De+tmert! of Pmasitology, AkJta Univ. School of Medicine, Akita, “‘Dqartmeat
Japan,
Departmen of Tropical Medicine, Jikei University School of Medicine.
Japan,
of Pathology, Beth Ismel Deacxmess Medic4 Center and Harvard
Tokyo. Japan.
Medical School, Boston USA
We previously reported that IgE responsiveness in mice is regulated &type specifically by a single autosomal gene not linked to H-2. The gene c~“Uols
Role of IL-3 and stem cell factor in nmasai agaimt intestinal hehninths was studied. wezc infeztcd eitha with S@~gr/oi&
mactcytosis and mucosal defencc
When “I& cellddicinrt
W/W” mice
rotti (S r) or S. Veneruelensis (S V),
expulsion of these parasites fmm the intestine was significantly delayed m-4 with that from normal littemmte +/+ mice. Delayed expulsion as well as defe&e i”testi”al mas( cell response in W/FV mice were normalized by bone marrow grafting.
Cmwu-sely, Sr-infcted ““de mice wae treated with murine U-3,
i”tcsti”al “ustocytosis was induced and the worms were expeled, so~esting
that
IL-3dcpcndcntly pmllfaated intestinal mast cells play a critical mle ir! expulsion of Slrongyloides spy.
7hi
concept was strengthened fmther by the fact that
expulsion of S v was delayed for 2 weeks in ILJ-knock defect was int&uc&
out mice. When IL-3-
into W/WVmice, S Y infection even persisted 0vQ 7 we=&.
These results suggest that both SCF and IL-3 are utilized i.n intestinal mast Cdl gmeration and mucosal defence agai”st intestinal parasites. Intestinal nustocytosis was i”doced by S Y infection in A/J and C58/J mice, of which bone “mmxv cells
capacity of IgE pmdwtior~ unrelated to antigens stimulated. Under this atopy gene,
strains of mice separated into IgE high and low responders. After T.spimlis infection. high respond.% (BALB/c. C3H, CDFl) produced larger amounts of lotal IgE and anti-T.spirohs IgE antibody than low responder(SJL). I@ dependencyof
protection to T.spiro/is was determined by comparison of the number of muscle larvae between IgEdeficient and IgE-producing conuol in each main. Selective IgE deficient mice were obtained by repealed injections of anti-IgEantibody. The IgE dependency of protection was found in IgE high responder suains but not in low responder strain. The effect of atopy gene orethe protection was confumed in backnoss
[(high-BALE/c x low-SJL)Fl x SJL] mice infected with T.sprralis. The
backcross mice segregated into IgE-high and low responders witi the ratio Of
I
I!
indicating a single gene. The number of muscle larvae recovered from IgE high
responders in backcross mice were signiiicanlly smaller than those of low
were non-m&tive to IL-3 in v&o due to a bra”& point nwlation in the IL-3Ra
responders. No significantly different number of muscle larvae was recoveredtram
gene. Sincz nmst cells could be induced from bone marrow cells of these mice by
both H-2 types of backcross mice, These results suggest that the alopy gene
co-presma
conuols protection to T.spirohs.
of IL-3 and SCF, S Y infection obviously stimulate in viva pmduc(ion
of these cytoki~~es. Our series of study indicate the inqortance of SCF and IL-3 in mast cell devdopment and parasite immunity