PMID- 11527407
OWN - NLM
STAT- MEDLINE
DCOM- 20011011
LR  - 20041117
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 286
IP  - 5
DP  - 2001 Sep 7
TI  - A factor of inducing IgE from a filarial parasite prevents insulin-dependent 
      diabetes mellitus in nonobese diabetic mice.
PG  - 1051-8
AB  - Parasitic helminth infections are characterized by eosinophilia and markedly 
      elevated levels of circulating antigen-nonspecific immunoglobulin E (IgE), 
      responses from which concern helminth protection. We previously purified a factor 
      from Dirofilaria immitis that induces antigen-nonspecific IgE in mice and rats. 
      Recombinant DiAg (rDiAg) has various biological activities. It is also known that 
      parasitic helminth infection generates tremendous Th2 responses. The nonobese 
      diabetic (NOD) mouse spontaneously develops Th1 cell-dependent autoimmune 
      diabetes. Here we investigated the effects of rDiAg on the initiation and 
      progression of this disease. rDiAg treatment of 6-week-old NOD females (the age 
      at which insulitis typically begins) completely prevented insulitis and diabetes. 
      Thus, rDiAg impaired the islet Ag-specific Th1 cell response in vivo, and the 
      prevention of diabetes by rDiAg was associated with switching of the response 
      from a Th1 to a Th2 profile. Since rDiAg clearly prevented insulitis by 
      inhibiting the development and further accumulation of pathogenic Th1 cells to 
      islets of Langerhans, we conclude that DiAg is a native Th2 inducer in filarial 
      helminth and that Th1 responses are required for early events in the development 
      of spontaneous autoimmune diabetes. In conclusion, the presence of parasitic 
      helminth infections may play an important role as an immunomodulator in some 
      autoimmune diseases or allergies.
CI  - Copyright 2001 Academic Press.
FAU - Imai, S
AU  - Imai S
AD  - Section of Environmental Parasitology, Department of International Health 
      Development, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima 
      Bunkyo-ku, Tokyo, 113-8519, Japan. sitimai@ac.mbn.or.jp
FAU - Tezuka, H
AU  - Tezuka H
FAU - Fujita, K
AU  - Fujita K
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Antigens, Helminth)
RN  - 0 (Autoantibodies)
RN  - 0 (Blood Glucose)
RN  - 0 (DiAg protein, Dirofilaria immitis)
RN  - 0 (Recombinant Proteins)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Amino Acid Sequence
MH  - Animals
MH  - Antigens, Helminth/*chemistry/immunology
MH  - Autoantibodies/chemistry
MH  - Blood Glucose/metabolism
MH  - Diabetes Mellitus, Type 1/*prevention & control
MH  - Dirofilaria/chemistry/immunology
MH  - Female
MH  - Humans
MH  - Immunoglobulin E/blood/*chemistry/immunology/metabolism
MH  - Mice
MH  - Mice, Inbred NOD
MH  - Molecular Sequence Data
MH  - Parasites/*chemistry
MH  - Rats
MH  - Recombinant Proteins/chemistry/metabolism
MH  - Sequence Homology, Amino Acid
MH  - Th1 Cells/metabolism
MH  - Th2 Cells/metabolism
MH  - Time Factors
EDAT- 2001/08/31 10:00
MHDA- 2001/10/12 10:01
CRDT- 2001/08/31 10:00
PHST- 2001/08/31 10:00 [pubmed]
PHST- 2001/10/12 10:01 [medline]
PHST- 2001/08/31 10:00 [entrez]
AID - S0006-291X(01)95471-3 [pii]
AID - 10.1006/bbrc.2001.5471 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2001 Sep 7;286(5):1051-8. doi: 
      10.1006/bbrc.2001.5471.