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Pathological manifestations in lymphatic filariasis correlate with lack of inhibitory properties of IgG4 antibodies on IgE-activated granulocytes.

Abstract Helminth parasites are known to be efficient modulators of their host's immune system. To guarantee their own survival, they induce alongside the classical Th2 a strong regulatory response with high levels of anti-inflammatory cytokines and elevated plasma levels of IgG4. This particular antibody was shown in different models to exhibit immunosuppressive properties. How IgG4 affects the etiopathology of lymphatic filariasis (LF) is however not well characterized. Here we investigate the impact of plasma and affinity-purified IgG/IgG4 fractions from endemic normals (EN) and LF infected pathology patients (CP), asymptomatic microfilaraemic (Mf+) and amicrofilaraemic (Mf-) individuals on IgE/IL3 activated granulocytes. The activation and degranulation states were investigated by monitoring the expression of CD63/HLADR and the release of granule contents (neutrophil elastase (NE), eosinophil cationic protein (ECP) and histamine) respectively by flow cytometry and ELISA. We could show that the activation of granulocytes was inhibited in the presence of plasma from EN and Mf+ individuals whereas those of Mf- and CP presented no effect. This inhibitory capacity was impaired upon depletion of IgG in Mf+ individuals but persisted in IgG-depleted plasma from EN, where it strongly correlated with the expression of IgA. In addition, IgA-depleted fractions failed to suppress granulocyte activation. Strikingly, affinity-purified IgG4 antibodies from EN, Mf+ and Mf- individuals bound granulocytes and inhibited activation and the release of ECP, NE and histamine. In contrast, IgG4 from CP could not bind granulocytes and presented no suppressive capacity. Reduction of both the affinity to, and the suppressive properties of anti-inflammatory IgG4 on granulocytes was reached only when FcγRI and II were blocked simultaneously. These data indicate that IgG4 antibodies from Mf+, Mf- and EN, in contrast to those of CP, natively exhibit FcγRI/II-dependent suppressive properties on granulocytes. Our findings suggest that quantitative and qualitative alterations in IgG4 molecules are associated with the different clinical phenotypes in LF endemic regions.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title plos neglected tropical diseases
Publication Year Start




PMID- 28742098
OWN - NLM
STAT- MEDLINE
DA  - 20170725
DCOM- 20170810
LR  - 20170813
IS  - 1935-2735 (Electronic)
IS  - 1935-2727 (Linking)
VI  - 11
IP  - 7
DP  - 2017 Jul
TI  - Pathological manifestations in lymphatic filariasis correlate with lack of
      inhibitory properties of IgG4 antibodies on IgE-activated granulocytes.
PG  - e0005777
LID - 10.1371/journal.pntd.0005777 [doi]
AB  - Helminth parasites are known to be efficient modulators of their host's immune
      system. To guarantee their own survival, they induce alongside the classical Th2 
      a strong regulatory response with high levels of anti-inflammatory cytokines and 
      elevated plasma levels of IgG4. This particular antibody was shown in different
      models to exhibit immunosuppressive properties. How IgG4 affects the
      etiopathology of lymphatic filariasis (LF) is however not well characterized.
      Here we investigate the impact of plasma and affinity-purified IgG/IgG4 fractions
      from endemic normals (EN) and LF infected pathology patients (CP), asymptomatic
      microfilaraemic (Mf+) and amicrofilaraemic (Mf-) individuals on IgE/IL3 activated
      granulocytes. The activation and degranulation states were investigated by
      monitoring the expression of CD63/HLADR and the release of granule contents
      (neutrophil elastase (NE), eosinophil cationic protein (ECP) and histamine)
      respectively by flow cytometry and ELISA. We could show that the activation of
      granulocytes was inhibited in the presence of plasma from EN and Mf+ individuals 
      whereas those of Mf- and CP presented no effect. This inhibitory capacity was
      impaired upon depletion of IgG in Mf+ individuals but persisted in IgG-depleted
      plasma from EN, where it strongly correlated with the expression of IgA. In
      addition, IgA-depleted fractions failed to suppress granulocyte activation.
      Strikingly, affinity-purified IgG4 antibodies from EN, Mf+ and Mf- individuals
      bound granulocytes and inhibited activation and the release of ECP, NE and
      histamine. In contrast, IgG4 from CP could not bind granulocytes and presented no
      suppressive capacity. Reduction of both the affinity to, and the suppressive
      properties of anti-inflammatory IgG4 on granulocytes was reached only when
      FcgammaRI and II were blocked simultaneously. These data indicate that IgG4
      antibodies from Mf+, Mf- and EN, in contrast to those of CP, natively exhibit
      FcgammaRI/II-dependent suppressive properties on granulocytes. Our findings
      suggest that quantitative and qualitative alterations in IgG4 molecules are
      associated with the different clinical phenotypes in LF endemic regions.
FAU - Prodjinotho, Ulrich F
AU  - Prodjinotho UF
AD  - Institute of Medical Microbiology, Immunology and Parasitology (IMMIP),
      University Hospital Bonn, Bonn, Germany.
FAU - von Horn, Charlotte
AU  - von Horn C
AD  - Institute of Medical Microbiology, Immunology and Parasitology (IMMIP),
      University Hospital Bonn, Bonn, Germany.
FAU - Debrah, Alex Y
AU  - Debrah AY
AD  - Kumasi Centre for Collaborative Research in Tropical Medicine (KCCR), Kwame
      Nkrumah University of Science and Technology, Kumasi, Ghana.
AD  - Faculty of Allied Health Sciences and School of Medical Sciences, Kwame Nkrumah
      University of Science and Technology, Kumasi, Ghana.
FAU - Batsa Debrah, Linda
AU  - Batsa Debrah L
AD  - Kumasi Centre for Collaborative Research in Tropical Medicine (KCCR), Kwame
      Nkrumah University of Science and Technology, Kumasi, Ghana.
AD  - Department of Clinical Microbiology, Kwame Nkrumah University of Science and
      Technology, Kumasi, Ghana.
FAU - Albers, Anna
AU  - Albers A
AD  - Institute of Medical Microbiology, Immunology and Parasitology (IMMIP),
      University Hospital Bonn, Bonn, Germany.
FAU - Layland, Laura E
AU  - Layland LE
AD  - Institute of Medical Microbiology, Immunology and Parasitology (IMMIP),
      University Hospital Bonn, Bonn, Germany.
FAU - Hoerauf, Achim
AU  - Hoerauf A
AD  - Institute of Medical Microbiology, Immunology and Parasitology (IMMIP),
      University Hospital Bonn, Bonn, Germany.
AD  - Bonn-Cologne Site, German Center for Infectious Disease Research (DZIF), Bonn,
      Germany.
FAU - Adjobimey, Tomabu
AU  - Adjobimey T
AUID- ORCID: http://orcid.org/0000-0002-4353-2897
AD  - Institute of Medical Microbiology, Immunology and Parasitology (IMMIP),
      University Hospital Bonn, Bonn, Germany.
AD  - Faculte des Sciences et Techniques (FAST), Universite d'Abomey-Calavi,
      Abomey-Calavi, Benin.
LA  - eng
PT  - Journal Article
DEP - 20170724
PL  - United States
TA  - PLoS Negl Trop Dis
JT  - PLoS neglected tropical diseases
JID - 101291488
RN  - 0 (Antibodies, Helminth)
RN  - 0 (Antigens, Helminth)
RN  - 0 (Cytokines)
RN  - 0 (Immunoglobulin G)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Animals
MH  - Antibodies, Helminth/*blood
MH  - Antigens, Helminth/immunology
MH  - Brugia malayi
MH  - Case-Control Studies
MH  - Cell Degranulation
MH  - Cytokines/immunology
MH  - Elephantiasis, Filarial/*immunology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Granulocytes/*immunology
MH  - Humans
MH  - Immunoglobulin E/*blood
MH  - Immunoglobulin G/*blood
MH  - Male
MH  - Middle Aged
MH  - Randomized Controlled Trials as Topic
MH  - Young Adult
PMC - PMC5542694
EDAT- 2017/07/26 06:00
MHDA- 2017/08/11 06:00
CRDT- 2017/07/26 06:00
PHST- 2017/01/16 [received]
PHST- 2017/07/05 [accepted]
PHST- 2017/08/03 [revised]
AID - 10.1371/journal.pntd.0005777 [doi]
AID - PNTD-D-17-00059 [pii]
PST - epublish
SO  - PLoS Negl Trop Dis. 2017 Jul 24;11(7):e0005777. doi:
      10.1371/journal.pntd.0005777. eCollection 2017 Jul.