AB10 Abstracts

SATURDAY

31

The Differential Relationship Between Regulatory T-Cells and

Age in Children with Food Allergy
Benjamin T. Prince, MD1, Kristin A. Erickson1, Christine
Szychlinski, MS, APN, CPNP2, Robert P. Schleimer, PhD, FAAAAI3,
Paul Bryce, PhD3, Anne Marie Singh, MD1,2; 1Division of Allergy-Immunology, Department of Pediatrics, Northwestern University Feinberg
School of Medicine, Chicago, IL, 2Division of Allergy-Immunology,
Department of Pediatrics, Ann & Robert H. Lurie Childrens Hospital
of Chicago, Chicago, IL, 3Division of Allergy-Immunology, Department
of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL.
RATIONALE: Regulatory T (Treg) cells are well known to play an
important role in the maintenance of self-tolerance, and patients who lack
these cells, such as in IPEX syndrome, have an increased incidence of
allergic disease. Although studies have highlighted differences in peripheral blood Treg populations of atopic adults, only a few conflicting studies
have examined differences in Tregs among children with allergic diseases.
METHODS: Peripheral blood mononuclear cells were isolated from 47
patients (0-18yrs) and analyzed using flow cytometry for CD3, CD4,
CD25, CD127, CCR6, and Foxp3. Populations of Tregs, defined as
CD4+CD25hiCD127loFoxp3+, were compared in food allergic children
and healthy controls using a 2-tailed Students t-test and linear regression
modeling.
_6yrs had significantly lower percentRESULTS: Food allergic children <
ages (p<0.05) of Tregs compared to healthy controls of similar age. This
difference was not observed in older children. There was a significant
decrease in both Treg cell percentages (p50.018, R50.584) and Treg
expression of Foxp3 (p50.012, R50.613) with age in healthy controls but
not in children with food allergy. Finally, food allergic children >6yrs had
significantly less Tregs expressing CCR6 (p<0.05), a gut-homing marker,
and this cell population significantly increased with age (p50.013,
R50.626) in healthy controls but not food allergic children.
CONCLUSIONS: Younger, food allergic children had significantly lower
percentages of Tregs compared to healthy controls, and this difference did
not persist with older children. This supports the hypothesis that early
childhood is likely a critical time in the development of normal immune
regulation and that Tregs are important in this process.

32

Glutathione S-Transferase Mu 1 (GSTM1) Gene Associated with

Allergic Rhinitis in a Food Allergy Cohort
Sheva K. Chervinskiy, DO1, Lisa Smeester2, Michael D. Kulis, Jr, PhD3,
David B. Peden, MD, MS, FAAAAI4, Brian P. Vickery, MD5, Rebecca C.
Fry, PhD6; 1Department of Pediatrics, University of North Carolina,
Chapel Hill, NC, 2Gillings School of Public Health, University of North
Carolina, Chapel Hill, NC, 3University of North Carolina School of Medicine, Chapel Hill, NC, 4Office #544, Campus Box 7310, University of
North Carolina at Chapel Hill School Medicine, NC, 5Department of Pediatrics, University of North Carolina, Chapel Hill, North Carolina, USA,
6
Gillings School of Public Health, University of North Carolina, Chapel
Hill NC.
RATIONALE: GSTM1 genes have been implicated in atopic inflammatory diseases. In this study, we explored whether GSTM1 genotype was
associated with food allergy phenotypes.
METHODS: Biospecimens from 100 randomly sampled food allergy
research subjects were collected for gene analysis. GSTM1 gene analysis
was carried out as previously described. We conducted a retrospective
chart review to collect phenotypic information, including past medical
history, number of allergic foods, serum specific IgE and food allergy
treatment response. Mann-Whitney and Chi-square analysis was
performed.
RESULTS: Of the 100 samples obtained, 81 subjects were successfully
genotyped, and 48/81 (x %) had a null GSTM1 genotype. Of the genotyped
subjects, 68 were successfully phenotyped via chart review. GSTM1 status
had no significant association with specific IgE, number of food allergies,
or response to food allergy treatment, as measured by food challenge
outcomes. There was no statistically significant association between

J ALLERGY CLIN IMMUNOL

FEBRUARY 2015

GSTM1 genotype with reported history of asthma or atopic dermatitis.

We found that patients with a GSTM1 genotype had a statistically
significant association with the incidence of allergic rhinitis in in this
cohort (p5 0.03).
CONCLUSIONS: In this cohort of food allergy patients, allergic rhinitis
was significantly associated with the GSTM1 genotype. This supports
previous studies revealing the association of this gene with allergic airway
disease. GSTM1 did not impact food allergy phenotype nor treatment
response to food allergy desensitization.

33

Disseminated Atypical Mycobacterial Infection in Three

Patients with Complete Digeorge Anomaly
Noah O. Agada, MD1, Suellen M. Yin, MD2, Jonathan S. Tam, MD2,
Matthew S. Kelly, MD1, M. Louise Markert, MD, PhD, FAAAAI1;
1
Duke University Medical Center, Durham, NC, 2Childrens Hospital
Los Angeles, Los Angeles, CA.
RATIONALE: Complete DiGeorge anomaly is a primary immunodeficiency characterized by athymia with fewer than 50 nave T cells/mm3
associated with either a cardiac defect or hypoparathyroidism.
Disseminated mycobacterial infection has not been described in these
patients. We present three cases of disseminated atypical mycobacterial
infection that developed among children with complete DiGeorge
anomaly.
METHODS: Clinical, laboratory, immunologic and radiologic data of
patients with complete DiGeorge anomaly referred to Duke University for
transplant were reviewed.
RESULTS: In patient 1 (P1), the diagnosis of disseminated mycobacterium avium complex (MAC) was made by lung biopsy 4 months after
thymus transplantation after a mass was noted on chest CT obtained to
evaluate for a source of fevers. P2 was diagnosed with MAC 2.4 months
after thymus transplantation from a mycobacterial blood culture obtained
for persistent fever. P2 was given steroids for possible immune reconstitution inflammatory syndrome when fevers recurred 18 days after starting
anti-mycobacterial therapy. In P3, a chest CT obtained to evaluate fevers
revealed lymphadenopathy and mycobacterial culture of a thoracic lymph
node biopsy grew Mycobacterium kansasii. P1 is on enteral medications
for MAC at 22 months post-transplantation and has normal T cell numbers.
P2 died 5 months after transplantation with finding of disseminated MAC
on autopsy. Flow cytometry revealed nave T cell development; the autopsy
showed thymopoiesis. P3 is 3 months post-transplantation, remains on
anti-mycobacterial treatment, and has not yet developed nave T cells.
CONCLUSIONS: Azithromycin or clarithromycin prophylaxis should be
considered for patients with complete DiGeorge anomaly. Aggressive antimycobacterial therapy without steroids is recommended.