In vitro generation of monocyte-derived dendritic cells with granulocyte–macrophage colony-stimulating factor and interleukin-4 was performed as previously described.15 B cells were then cultured as 1 × 106 cells/well in a 24-well flat-bottom culture dish in X-Vivo 15 serum-free cell culture medium (Cambrex, Charles City, IA). To test the shaving reaction, RTX

antibody (MabThera® from Roche, Basel, Switzerland) was added in a final concentration of 5 μg/ml. Syngeneic monocytes were added in titrated numbers up to 1 × 106 cells/well. After 18 hr, cells were harvested and labelled with relevant antibodies for flow cytometry. AZD9668 Based on flow cytometry data, mean fluorescence intensity (MFI), % shaving was defined as (1 − [MFI of monocyte containing RTX sample − MFI of monocyte containing isotype control/MFI of RTX sample − MFI of isotype control]) × 100. Cells from co-cultures were labelled with FITC-conjugated anti-RTX antibody (Clone MB2 A4 from AbD Serotec, Dusseldorf, Germany) or a relevant isotype control (IgG2a) and the effect of RTX was tested. Related antibody combinations where used when testing alternative anti-CD20 antibodies.

After labelling and washing, Regorafenib cells were resuspended in PBS containing 1% BSA as running buffer and directly analysed on a FACSCalibur (San Jose, CA) using bd cell quest pro software (Becton Dickinson, Franklin Lane, NJ). Analyses of monocytes and B cells were separated using gates defined by forward and side scatter. In separate experiments, cell viability including the effect of CDC was tested

with a commercial kit from BD (Becton Dickinson) using FITC-annexin V and propidium iodide. Human IgG was from Sigma (St Louis, MO), anti-CD14 and anti-CD64 was from BD. Type I and type II anti-CD20 antibodies were a kind gift from Mark S. Cragg and Claude H.T. Chan. In experiments, testing the effect of hyperosmolar sucrosis, 0·4 m sucrosis (Sigma) was added to the monocyte–B-cell co-culture. Similarly, 80% active human AB serum was used when testing CDC. In experiments with blockade of protease activity, 10 mm EDTA (Sigma) was used and 3 mm PMSF, 2·8 mg/ml aprotinin, 20 nm bestatin hydrochloride, 5 mm 3-mercaptopyruvate sulfurtransferase 1,10-phenanthroline monohydrate, 5 μm phosphoramidon disodium salt and 5 μg/ml α2-macroglobulin (all from Sigma) were used for inhibition of specific classes of proteases. Monocyte-mediated shaving of RTX/CD20 complexes from the surface of CD20+ cells has recently been reported as a major obstacle for RTX treatment in haematological malignancies.13 Our results here confirm the shaving reaction and demonstrated monocyte-mediated shaving of RTX antibody from the surface of CD19+ B cells. This phenomenon was monocyte number-dependent, not evident with 1 × 104 monocytes, increased at 1 × 105 and almost complete after the addition of 4 × 105 to 5 × 105 monocytes (Fig. 1).

In the absence of exogenous factors, however, CD3-crosslinking in primary T cells results in proliferation without development of effector function, although the activated CD4+ and CD8+ T cells produce IL-2 and IFN-γ, respectively. Th1 cells mediate responses against intracellular pathogens and secrete their signature cytokine, IFN-γ. IL-4 is the

signature cytokine of Th2 cells, which are involved in immunity against extracellular parasites, including helminthes. Th17 cells, Pembrolizumab purchase as its name implies, secrete IL-17 and are important for immunity against extracellular bacteria and fungi 19. In addition, these cells have been implicated in various autoimmune diseases, such as experimental autoimmune encephalomyelitis, collagen-induced arthritis 17 and systemic lupus erythematosus 20, although recent reports have described a protective role for IL-17A in inflammatory bowel disease (IBD) 21–23. Here we report that in the absence of DPP2, CD4+ T cells Quizartinib respond to CD3 crosslinking by hyper-proliferation and secretion of IL-17, in the absence of any exogenous factors. The same profile was observed after in vivo priming and in vitro antigen-specific restimulation of the T cells. These data suggest that IL-17

production is the default program for T-cell differentiation in the absence of DPP2. Thus, DPP2 seems to prevent quiescent T cells from spontaneously drifting into cell cycle by imposing a threshold. To examine the role of DPP2 in vivo, we generated genetically deficient DPP2

mice, using two lentiviral vectors for conditional, Cre-lox-regulated, RNA interference (RNAi) 24. One vector allows for conditional activation (pSico), whereas the other permits conditional inactivation (pSicoR) of short hairpin RNA (shRNA) expression (Fig. 1A and B). Various shRNA sequences designed against mouse DPP2 were cloned into the pSicoR and pSico lentiviral vectors and tested for their effectiveness in reducing DPP2 expression (Supporting Information Fig. 1). The shRNA sequence with the most significant DPP2 kd was selected and used to infect ES cells and ultimately Cytidine deaminase generate chimeric DPP2 kd mice. The constitutive DPP2 kd mouse (Fig. 1A), which expresses the shRNA against DPP2 in all tissues, was embryonic lethal, because only three chimeric mice were generated with extremely low chimerism (5–15%), based on coat color and GFP expression. These results were anticipated due to the fact that several previous attempts to generate a traditional DPP2 ko mouse had failed. In contrast, numerous, highly chimeric (90–95%) conditional DPP2 kd mice were generated (Fig. 1B). These mice were crossed to lck-Cre tg mice 25, resulting in T-cell-specific DPP2 kd, originating at the double-negative stage in thymocyte development, termed lck-DPP2 kd mice.

In this study we report that the proinflammatory cytokines interleukin (IL)-2, interferon (IFN)-γ and tumour necrosis factor (TNF)-α show a time-dependent increase upon ex-vivo bacterial, viral and fungal antigen stimulations. Furthermore, evidence is provided that this assay is sensitive to mirror stress hormone-mediated immune modulation in humans as shown either after hydrocortisone injection or after acute

stress exposure during free fall in parabolic flight. This in-vitro test appears to be a suitable assay to sensitively mirror stress hormone-dependent inhibition of cellular immune responses in the human. HM781-36B in vivo Because of its standardization and relatively simple technical handling, it may also serve as an appropriate research

tool in the field of psychoneuroendocrinology in clinical as in field studies. Humans are continuously subjected to environmental challenges which affect the immune function according to the intensity of psychological and physiological stressors. Due to the complex nature of in-vivo immune responses, the delayed-type hypersensitivity (DTH) skin test has served as a standardized tool to monitor the overall status of the immune system by simultaneously placing six antigens and one diluent (as a negative control) intracutaneously into the forearm. With the DTH skin test it was possible to Carfilzomib evaluate, to a certain degree, the extent of immunodeficiency, as seen in individuals infected with the human immunodeficiency virus (HIV) [1].

In addition to being used as a clinical investigative tool in immune deficiency states, the DTH skin test was also used widely to monitor immune function in states of psychological stress and psychiatric illness. Declines in immune function were found in subjects suffering from severe depression [2, 3], in Demeclocycline crews wintering in the Antarctic [4, 5] and individuals experiencing perceived distress [6-9]. In 2002 this in-vivo skin test (multi-test CMI; Mérieux, Lyon, France) was removed from the market, in part because of the risk of antigen-sensitization when applied repeatedly to the same individual. After the DTH skin test was phased out, no such alternative tests were available to evaluate overall immunity. Standardized in-vitro methods such as the lymphocyte transformation test [10] and in-vitro cytokine induction [11] are used for the measurement of antigen-dependent T cell responses, but these tests are complicated in their performance and may not mirror the immune responses to the pathogenic spectrum that the DTH skin test was able to recall. Even though the complex skin reaction of the DTH skin test – which includes, e.g. cell migration – cannot be reproduced fully in a whole-blood in-vitro system, DTH reactions also seem possible to be reflected in blood tests [12, 13].

After 30 min, the blocking solution was discarded, and cell suspensions at various

dilutions were added to wells and incubated at 37 °C for 4 h under 5% CO2 in moist air. The cells were washed and then incubated with horseradish peroxidase-conjugated goat anti-mouse heavy chain α-specific antibodies (Southern Biotechnology Associates) at 4 °C for 20 h. Following incubation, the plates were washed with PBS and developed adding 3-amino-9-ethylcarbazole dissolved in 0.1 M sodium acetate buffer containing H2O2 to each well (Moss, Inc.). Plates were incubated at room temperature for 30 min and washed with distilled water, and AFCs were then counted with the aid of a stereomicroscope (Olympus, Tokyo, Japan). Mononuclear cells were isolated 7 days after the final immunization from submandibular lymph nodes (SMLs) of the immunized mice, adjusted selleck compound to a concentration of 5 × 106 cells mL−1, and cultured with 5 μg mL−1 of 25k-hagA-MBP in RPMI-1640 medium containing 10% fetal bovine serum, 50 μM 2-mercaptoethanol, 15 mM HEPES, 2 mM l-glutamine, 100 U mL−1 penicillin, 100 μg mL−1

streptomycin, and 10 U mL−1 of recombinant IL-2 (Genzyme, Cambridge, MA). Cultures were incubated for 4 days at 37 °C under 5% CO2 in air. To measure the 25k-hagA-MBP-specific cell proliferation, 1.0 μCi of [3H]thymidine was Selleck Temsirolimus added to the culture 18 h before harvesting, and the incorporated radioactivity was measured by scintillation counting. Four-day culture supernatants were also collected and centrifuged to remove cell debris. The IL-4, IFN-γ, and TGF-β cytokine levels of the culture supernatants were then determined by cytokine-specific ELISA kit (Pierce Endogen; Pierce Biotechnology, Rockford, IL) as described previously (Hashizume et al., 2008). Mice were orally infected

with P. gingivalis as described previously (Du et al., 2011), with minor modifications. Briefly, mice were given ad libitum access to ionized water containing sulfamethoxazole/trimethoprim (Sulfatrim; Goldline Laboratories, Fort Lauderdale, FL) at 10 mL per pint for 10 days. This was followed by a 3-day antibiotic-free period. Mice were then administered 109 CFU of P. gingivalis suspended in 100 μL of PBS with 2% carboxymethylcellulose this website via oral topical application. Mice were inoculated five times a week (from Monday to Friday) for 3 weeks, for a total of 15 inoculations. Control groups included sham-infected mice, which received antibiotic pretreatment and carboxymethylcellulose without P. gingivalis. Horizontal bone loss around the maxillary molars was assessed by the morphometric method as described previously (Klausen et al., 1989). The distance from the cementoenamel junction (CEJ) to the alveolar bone crest (ABC) was measured at a total of 14 buccal sites per mouse.

The authors have no conflicts of interest to disclose. “
“Citation Wira CR, Patel MV, Ghosh M, Mukura L, Fahey JV. Innate immunity in the human female reproductive tract: endocrine regulation of endogenous antimicrobial protection against HIV and other sexually transmitted infections. Am J Reprod Immunol 2011; 65: 196–211 Mucosal surfaces of the female reproductive tract (FRT) contain a spectrum of antimicrobials that provide the first line of defense against viruses, selleck compound bacteria, and fungi that enter the lower FRT. Once thought to be a sterile compartment, the upper FRT is periodically exposed to pathogens throughout the menstrual cycle. More recently, secretions from the upper FRT have

been shown to contribute to downstream protection in the lower FRT. In this review, we examine the antimicrobials in FRT secretions made by immune cells and epithelial cells in the upper and lower FRT that contribute to innate protection. Because each site is hormonally regulated to maintain

fertility, this review focuses on the contributions of hormone balance during the menstrual cycle to innate immune protection. As presented in this review, studies from our laboratory and others demonstrate that sex hormones regulate antimicrobials produced by innate immune cells throughout the FRT. The goal of this review is to examine the spectrum of antimicrobials in the FRT and the ways in which they are regulated to provide protection against pathogens that compromise reproductive

Linsitinib mw health and threaten the lives of women. Sexually transmitted infections (STI) are a major worldwide health problem.1 Despite extensive efforts, only limited success has been achieved Farnesyltransferase in dealing with a growing list of STI that include bacteria (group B streptococcus, Neisseria gonorrhoeae, Chlamydia trachomatis, Treponema pallidum), parasites (Trichomonas vaginalis), and viruses [herpes simplex (HSV), human papilloma (HPV) and human immunodeficiency (HIV) virus]. Taken together, more than 20 pathogens, all of which are transmissible through sexual intercourse, account for approximately 340 million new STI cases annually.2 Since 1975, HIV has accounted for approximately 25 million deaths with an additional 33.4 million people (of which approximately 50% are female) currently infected worldwide.3 In sub-Saharan Africa, the area hardest hit by the pandemic, women living with HIV/AIDS make up approximately 60% of the number of HIV-infected people.3 Depending on the African country analyzed, infection rates vary from 5 to 25% of the population. Not widely recognized are recent findings that major cities in the United States such are Washington DC have infection rates (approximately 3%) that are comparable to those seen in Africa.4 The mucosal surfaces of the human FRT are protected against pathogens by both the adaptive and the innate immune systems.

© 2011 Wiley Periodicals, Inc. MS-275 mw Microsurgery, 2011 “
“Reconstruction of the great toe defect is difficult. The most distal point of the rotation arc of a retrograde-flow medial plantar flap is the plantar side of the proximal phalanx. The purpose of this report was to present a new procedure that extends the rotation arc of this flap. Results of anatomic study and application in two patients were presented. An anatomical study was conducted on 10 freshly frozen cadavers to determine the rotation arc of the medial plantar flap based distally on the lateral plantar vessels. To enable anterograde venous drainage, two accompanying veins of the vascular

pedicle were separated and

anastomosed to each other. This surgical procedure was implemented in two clinical cases with the great toe defect. The maximum size of the elevated AZD2014 supplier flap was 4 × 7 cm. The status of venous congestion of the flap was determined using the blood glucose measurement index. We confirmed that the rotation arc of the medial plantar flap based distally on the lateral plantar vessels could reach the tip of the great toe, preserving all lateral plantar nerves and plantar metatarsal arteries. In the two cases, the congestion of the flap improved with anterograde venous drainage and the flaps survived completely. A pedicled medial plantar click here flap with anterograde venous drainage may be a useful alternative option for the reconstruction of relatively large great toe defects. © 2014 Wiley Periodicals, Inc. Microsurgery 34:398–403, 2014. “
“Pneumatic perforation of the esophagus caused by blast injury is very rare. Our patient presented with esophageal stricture in the context of a previous reconstruction of an esophageal rupture secondary to a distant air-blast injury. The ruptured esophagus was initially reconstructed with

a left pedicled colon interposition in an antiperistaltic pattern. However, dysphagia developed 4 years later because of severe reflux-induced stenosis at the junction of the cervical esophagus and the left pedicled colon segment. A free isoperistaltic jejunal flap was performed to replace the cervical esophagus, with an anti-reflux Roux-en-Y colojejunostomy between the caudal segment of the left pedicled colon and the jejunum. The patient was discharged uneventfully 29 days later with smooth esophageal transit and no further reflux, as shown by scintigraphic scan. Esophageal reconstruction in an isoperistaltic pattern using a free isoperistaltic jejunal flap combined with an anti-reflux Roux-en-Y colojejunostomy has never been reported in the literature and appears to be an effective method to provide smooth passage of food and prevent restenosis of the esophagus. © 2011 Wiley-Liss, Inc. Microsurgery, 2011.

270 IMPACT OF CINACALCET PRESCRIPTION PRE-TRANSPLANT ON MINERAL METABOLISM IN RENAL TRANSPLANT RECIPIENTS AK SHARMA1,2, R MASTERSON1,2, SJ TAN1,2, P HUGHES1,2, SG HOLT1,2, ND TOUSSAINT1,2 1Department of Nephrology, The Royal Melbourne Hospital, Parkville, Victoria; 2Department of Medicine (RMH), The University of Melbourne, Parkville, Victoria, Australia CH5424802 clinical trial Aims: To

determine the effect of the calcimimetic cinacalcet, administered to dialysis patients pre-transplantation, on post-transplant biochemical markers of mineral metabolism. Background: Cinacalcet was approved in Nov 2007 for treating secondary hyperparathyroidism (SHPT) in dialysis patients. Reports on biochemical profiles and clinical outcomes in patients discontinuing cinacalcet at the time of transplantation are limited. Methods: A single-centre retrospective analysis over 10 years to study markers of mineral metabolism in renal transplant recipients (transplanted Jan 2002–Dec 2011). We assessed changes of biochemical parameters with the introduction of cinacalcet, and compare patients discontinuing

cinacalcet at the time of transplantation with this website cinacalcet-naïve patients. Results: 696 transplants were performed over 10 years. Mean age of patients was 47.4 years, 64.8% male, 94 (13.5%) patients with graft loss and 29 deaths (4.2%). Since Nov 2011 377 patients have been transplanted, 18.4% having had cinacalcet pre-transplant. No significant differences were seen in markers of

mineral metabolism at 12mths post-transplant in the pre- and post-cinacalcet eras. At time of transplantation, parathyroid hormone (PTH) levels were higher in those on cinacalcet vs cinacalcet-naïve patients (48.5 ± 31.5 vs 31.2 ± 22.8 pmol/L, P = 0.003). 12 month post-transplant serum calcium was significantly higher (2.50 ± 0.2 vs 2.45 ± 0.16 mmol/L, P = 0.04) and PTH higher, although not significantly, (12.0 ± 12.4 vs 9.4 ± 7.9 pmol/L, Urease P = 0.10) for those previously administered cinacalcet. No difference in renal function at 12 months (mean eGFR 53.6 ± 17.4 mL/min/1.73 m2) was observed between cinacalcet patients and cinacalcet-naïve patients. Conclusion: Biochemical profiles suggest minimal changes to markers of post-transplant mineral metabolism with the introduction of cinacalcet. Renal transplant recipients discontinuing cinacalcet at the time of transplantation had slightly increased serum calcium and PTH at 12 months although this may not be clinically significant.

After blocking FcR, cells were incubated with appropriately diluted antibodies. Acquisition was performed using a FACSort or a LSRII (BD Biosciences, Mountain View, CA, USA) and data analysis was conducted

using FlowJo software (Tree Star, Ashland, OR, USA). Comparisons of two groups of data were analyzed by two-tailed Student’s t-test using GraphPad Prism 4.0. (GraphPad, San Diego, CA, USA). This project has been funded in whole or in part with federal funds from the National Cancer Rapamycin Institute, National Institutes of Health, under contract HHSN261200800001E. This Research was supported (in part) by the Intramural Research Program of the NIH, National Cancer Institute, Center for Cancer Research. R. H. is supported by International Training Program of Japan Society for the Promotion of Science. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. The authors thank Dr. Teresa Born and Dr. John E Sims XAV-939 clinical trial at Amgen Inc. for providing

anti-mouse TNF antibody and isotype control Mu IgG, and Dr O. M. Zack Howard, Dr. Hong Lou, Dr Hongchuan Li and Dr Gonzalo M. de la Rosa for help in this study. Conflict of interest: The authors declare no financial or commercial conflict of interest. “
“The activation-induced cytidine deaminase (AID) mediates somatic hypermutation and class switch recombination of the Ig genes by directly deaminating cytosines to uracils. As AID causes a substantial amount of off-target mutations, its activity has been associated with lymphomagenesis and clonal evolution of B-cell malignancies. Although it has been shown that AID is

expressed in B-cell chronic lymphocytic leukemia (CLL), a clear analysis of in vivo AID activity in this B-cell malignancy remained elusive. In this study performed on primary human CLL samples, we report that, despite the presence of a dominant VDJ heavy chain region, a substantial intraclonal diversity was observed at VDJ as well as at IgM switch regions (Sμ), showing ongoing AID activity in vivo during disease progression. This AID-mediated heterogeneity was higher in CLL subclones expressing CD86, which we identified as the proliferative CLL fraction. Finally, CD86 expression Proteases inhibitor correlated with shortened time to first treatment and increased γ-H2AX focus formation. Our data demonstrate that AID is active in CLL in vivo and thus, AID likely contributes to clonal evolution of CLL. “
“The ontogenic relationship between pro-inflammatory populations of interleukin-17 (IL-17A)- and/or IL-22-producing T cells and other T-cell subsets is currently unclear in humans. To appreciate T helper cell-lineage commitment, we combined cytokine production profiles of in vitro expanded T-cell clones with T-cell receptor (TCR) clonotypic signatures.

This may possibly be due to a shortened G1 phase caused by DPP2 kd, an observation that we made in DPP2 kd fibroblasts, which proliferate faster than WT cells in the presence of serum (unpublished result). Similarly, it has been reported that T cells lacking transactivator of ErbB2 (TOB1) have a reduced threshold of activation 34. Furthermore,

loss of Lung-Kruppel-like this website factor 2 (KLF2) leads to a loss of quiescence defined by proliferation, increased metabolism and altered expression of activation markers 35. Interestingly, we previously demonstrated that DPP2 is transcriptionally activated by KLF2 and TOB1, linking them in a program that maintains lymphocyte quiescence, which is regulated by quiescence-specific transcription 3. Collectively, these data support the role of DPP2 in preventing proliferation and promoting quiescence. Bortezomib manufacturer Of particular interest is the finding that naïve T cells from lck-DPP2 kd mice mainly produce IL-17, the signature cytokine of Th17 cells 36, upon TCR-mediated activation in vitro. In addition, these cells significantly upregulate rorγt mRNA, the master

regulator of Th17 differentiation 15. In agreement with this observation, we found that IL-2 and IFN-γ production was downregulated in the activated mutant T cells. CD4+ and CD8+ T cells respectively, produce these cytokines after TCR activation in the absence of exogenous

factors. Furthermore, IL-2 has been shown to induce Foxp3 expression and inhibit Th17-cell differentiation 37. Collectively, our data support the notion that loss of DPP2 causes T cells to differentiate into Th17 cells and IL-17 producing CD8+ T cells upon TCR stimulation. It can be surmised from these results that the PRKD3 production of the inflammatory cytokine IL-17 is the default pathway in T-cell differentiation and is actively suppressed by DPP2. Such a control may be important to prevent expansion of autoreactive T cells. In agreement with this hypothesis, we observed increased levels of ANA in the lck-DPP2 kd mice, indicative of augmented autoantibody production in these mice. Th17 cells have been implicated in numerous human diseases, such as psoriasis, rheumatoid arthritis, multiple sclerosis, asthma and some bacterial and fungal infections 38. A recent report on the effects of the loss of early growth response gene-2 in T cells suggests that autoimmune disorders can result from a loss of effector T-cell expansion and inflammatory activation 39. This is consistent with the observations made in lck-DPP2 kd mice, where T cells are hyper-proliferative and differentiate into IL-17-producing cells. Several other reports have also shown examples of proteins that act to prevent abnormal T-cell proliferation and autoimmunity associated with the production of IL-17.

This study was supported by the Key Project of Chinese National Programs (2008ZX10003-010), National Natural Science Foundation of China 30670108 and J0730860, RFDP20060246037, and the Intramural Research Program of

the National Institute of Allergy and Infectious Diseases, The National Institutes of Health, USA. C.W. and J.F. contributed equally to this work. “
“Immunoassay designs rely on the great specificity of antibodies and a suitable marker that facilitates generation of a quantitative signal. Currently, PD-1/PD-L1 inhibitor there is no reliable method for measuring the titers of an anti-idiotypic antibody. Our initial attempt to measure titers of mouse anti-idiotypic antibody after idiotypic vaccination with HM-1 killer toxin neutralizing monoclonal antibody (nmAb-KT) failed.

Because the injected antigen, nmAb-KT, is a mouse IgG, using a commercial antibody to measure the antibody titer always gave a false positive signal against control mouse serum antibody in parallel with the antigen-treated immunized serum antibodies. To get a reliable and clearly differentiable signal by ELISA, idiotypic antigen was labeled with HRP and HRP-conjugated-nmAb-KT used to measure the antibody titers in the antigen-treated mice. Compared with control mice, signals were found in high anti-nmAb-KT IgG responses in test mice; however, Sunitinib solubility dmso untreated control mice had a significant amount of purified non-specific IgG. This method is amenable to long read lengths and will likely enable anti-idiotypic antibody titer measurement in a more specific and cost effective way without requiring commercial antibody. “
“This study aimed to comprehensively describe inflammatory responses to trivalent influenza virus vaccine (TIV) among pregnant women and determine whether responses differ compared to non-pregnancy. Twenty-eight pregnant and 28 non-pregnant women were vaccinated. Serum cytokines were measured at baseline, and 1, 2, and 3 days post-vaccination. Anti-influenza antibody titers were measured at baseline and 1 month post-vaccination.

Overall, following vaccination, tumor necrosis factor (TNF)-α Niclosamide and interleukin(IL)-6 increased significantly, peaking at 1 day post-vaccination (P’s < 0.001). Pregnant versus non-pregnant women showed no differences in IL-6, TNF-α, or IL-1β responses. Pregnant women showed no change in IL-8 and increases in migration inhibitory factor (MIF), while non-pregnant showed decreases in both. Pregnancy did not significantly alter antibody responses. Inflammatory responses to TIV are mild, transient, and generally similar in pregnant and non-pregnant women. Given the variability evidenced, vaccination may provide a useful model for studying individual differences in inflammatory response propensity. "
“One morning last December on my way to work, something strange happened.