Considering the role of CD146 in lymphocyte/endothelial interactions [9], CD146 expression might correlate with adhesion and homing

markers. Expression of the proinflammatory chemokine receptor, CCR5, varied between HDs. Within the CD4, but not the CD8 subset, CCR5+ cells were over-represented on CD146+ T cells (Fig. 10). The expression of CXCR3, another chemokine receptor, also varied between donors, independently of CD146 expression (Supporting information, Fig. S7). HD CD4 and CD8 T cells expressed CD31/platelet endothelial cell adhesion molecule (PECAM) (Supporting information, Fig. S8) and CD54/ intercellular adhesion molecule 1 (ICAM-1) (Supporting information, Fig. S9) at varying frequencies. CD146+ HD CD4 T cells, but not CD8 cells, were depleted click here slightly but systematically of CD31+ cells, and very Deforolimus slightly enriched for CD54+ cells. Throughout this study, dead cells were only excluded by scatter; non-specific binding of isotype control antibody to 0·1–0·2% of cells was seen in some experiments (Fig. 1). However, CD4 and CD8 cells differed in their co-expression patterns; some markers were enriched whereas others

were depleted, and the associations between CD146 and other markers in CD4+ T cells were consistent between donors and, where previously studied, consistent with earlier work. Taken together, the results are not explained by non-specific staining. Surprisingly few CTD patients showed evidence of CD146 up-regulation BCKDHB ex vivo (Fig. 3). The median frequency of CD146+CD4+ T cells remained normal in patients with SLE (1·60%), SSc (2·0%) and pSS (1·80%; one patient was just above the normal range). In contrast to previously described patients with SLE and pSS [30-32], including patients from our CTD clinic (C. Bryson and F.C. Hall, unpublished data), these patients showed no T cell activation or derangement of memory subsets or adhesion markers (Figs 4-10 and Supporting information, Figs S4–S9, middle panels). In these patients, systemic T cell dysregulation appeared to be minor or well controlled by therapy. This contrasts with

other studies of blood T cell activation in patients with SLE or pSS, with implications for the interpretation of our results (see Discussion). In contrast, the five sSS patients in our study had significantly increased CD146 expression on CD4 cells (median: 4·0%) and, to a lesser extent, on CD8 cells (Fig. 3). These patients harboured elevated frequencies of CD4 and CD8 cells expressing the activation markers CD25 and OX-40 (Figs 4 and 5; asterisks symbolize significant differences from HDs or other CTD groups by non-parametric anova). Moreover, the correlation of CD146 with activation markers was more extensive in the sSS patients. In all five patients, each of the activation markers tested (CD25, HLA-DQ, OX-40, CD69 and CD70) was over-represented in the CD146+ subpopulation of CD4 cells (Figs 4-6, Supporting information, Figs S4 and S5).

Twenty Hebrew-learning infants aged 8 to 11 months were presented with lists of nonsense words featuring the first two patterns (Experiment 1), and 20 were presented with nonsense

words featuring the second two patterns (Experiment 2). The results showed longer listening to CéCeC than to CóCoC lists and to CaCóC than to CaCéC lists, suggesting that infants recognized the common nonadjacent vocalic patterns in both cases. The study thus demonstrates that Hebrew-learning infants are able to disregard see more the intervening consonants within words and generalize their vocalic pattern to previously unheard nonwords, whether this pattern includes identical or different

vowels and regardless of the rhythmic pattern of the word (trochaic or iambic). Analysis of the occurrence of the relevant vowel patterns in input speech in three Hebrew corpora (two addressed to children and one to adults) suggests that exposure to these patterns in words underlies the infants’ preferences. ZD1839 manufacturer “
“The ability to effectively regulate emotions is a critical component of early socio-emotional development. This longitudinal study examined the developmental trajectories of emotion regulation in a sample of 3-, 5-, and 7-month-olds during an interaction with mothers and fathers. Infants’ negative affect and use of behavioral strategies, including distraction,

self-soothing, and high intensity motor behaviors were rated during the still-face episode of the Still-Face Paradigm. Longitudinal mixed-effects models were tested to determine whether strategies were followed by an increase or decrease in negative affect. Results from mother-infant and father-infant dyads indicated that focusing attention away from the unresponsive parent and engaging in self-soothing behaviors were associated with a subsequent decline in negative affect and the strength of these temporal associations were stable across infancy. In contrast, high-intensity motor behaviors were followed by an increase in negative affect Erastin mouse and this effect declined over time. No significant effects were found for the behavioral strategy of looking at the parent. Results underscore the importance of considering infant age and the social partner when studying the effectiveness of emotion regulatory strategies in early infancy. “
“We examined how infants’ categorization is jointly influenced by previous experience and how much they shift their gaze back and forth between stimuli. Extending previous findings reported by K. A. Kovack-Lesh, J. S. Horst, and L. M.

Here, we report that PstS1 exclusively activated memory T cells but did not stimulate naïve cells. Thus, the ability of PstS1 to induce expression of co-stimulatory molecules and/or release of IL-6 and IL-1β by DCs, as better discussed below, may account for the Ag-independent activation of memory T lymphocytes. However, although unlikely, a contribution for TCR cross-reactivity, which may exist even between apparently unrelated peptide Ag [35] cannot

be excluded. Activation of T lymphocytes by unrelated Ags occurs frequently during infectious processes but the significance of this phenomenon is still a matter of debate. It is thought to be involved in homeostatic turnover, maintenance of immunological memory, or amplification of inflammatory responses [36]. PstS1 is released by replicating Mtb, especially during the acute phase of infection, as indicated by increased levels of anti-PstS1 mAbs in the sera of see more most patients with multibacillary or advanced pulmonary TB [37, 38]. Therefore, PstS1

released by Mtb may be exploited by the bacterium itself to facilitate inflammation during active TB disease. It may promote IFN-γ, IL-17, and IL-22 release by memory T cells specific for other Mtb Ags, such as Ag85B and Ag85A. IFN-γ and IL-17 are induced during primary TB [2-6] and are both capable of inducing chemokines that promote cell recruitment and granuloma organization throughout infection [39]. While many clinical and experimental data indicate a central role for the IFN-γ response in protection Atezolizumab manufacturer against Mtb infection, the role of IL-17 is not yet fully elucidated. Th17 cells per se may contribute to the early control of Mtb infection, although they may increase tissue damage [4, 5]. Similarly, IFN-γ-producing T cells may directly cause lung damage and may alter the efficacy of protective TB

immunity unless tightly controlled [9, 10, 40], suggesting that excessive activation of IFN-γ response may be deleterious for the host. Thus, during TB infection, a balance between Th1 and Th17 responses Arachidonate 15-lipoxygenase needs to be achieved so as to control bacterial growth and limit immunopathology. Recently, a growing body of evidences suggests a role for IL-22 in TB. In healthy humans exposed to mycobacteria, IL-22-expressing CD4+ T cells were reported as being distinct from Th17 and Th1 cells [41]. Moreover, unlike IL-17, IL-22 was found in BALF of TB patients, suggesting that these two cytokines may have distinct roles in TB infection and disease outcome [41, 42]. Nevertheless, considering that the amplification of IFN-γ, IL-17, and IL-22 responses are a double-edge sword for the host [6-10, 42], further investigations are required to determine whether PstS1 release during infection is of benefit to the host or the mycobacteria. Moreover, it remains to be elucidated whether induction and amplification of Ag-unrelated memory Th1 or Th17/22 responses mediated by PstS1 are short term or long lasting.

We thank Ministerio de Educación y Ciencia and FECYT (Spain) for a postdoctoral fellowship to O. Palomares. Conflict of interest: The authors declare no financial or commercial conflict of interest. “
“Citation Rosenberg VA, Buhimschi IA, Dulay AT, Abdel-Razeq SS, Oliver EA, Duzyj CM, Lipkind H, Pettker CM, Buhimschi CS. Modulation of amniotic fluid activin-A and inhibin-A in women with preterm premature rupture of the membranes and infection-induced preterm birth. Am J Reprod Immunol 2012; 67: 122–131 Problem  Activins and inhibins are important modulators of inflammatory processes. We explored activation of amniotic fluid (AF) activin-A and inhibin-A system in women with intra-amniotic

infection and preterm

premature rupture of the membranes (PPROM). Method of study  We analyzed 78 AF samples: ‘2nd trimester-control’ (n = 12), ‘3rd trimester-control’ https://www.selleckchem.com/products/pci-32765.html (n = 14), preterm labor with intact membranes [positive-AF-cultures (n = 13), negative-AF-cultures (n = 13)], and PPROM [positive-AF-cultures (n = 13), negative-AF-cultures (n = 13)]. Activin-A levels were evaluated ex-vivo following incubation of amniochorion and placental villous explants with Gram-negative lipopolysaccharide (LPS) or Gram-positive (Pam3Cys) bacterial mimics. Ability of recombinant activin-A and inhibin-A to modulate inflammatory reactions in fetal membranes was explored through explants’ IL-8 release. CHIR-99021 chemical structure Results  Activin-A and inhibin-A were present in human AF and were gestational age-regulated. Activin-A

was significantly upregulated by infection. Lower inhibin-A levels were seen in PPROM. LPS elicited release of activin-A from amniochorion, but not from villous explants. Recombinant activin-A stimulated IL-8 release from amniochorion, an effect that was not reversed by inhibin-A. Conclusion  Human AF activin-A and inhibin-A are involved in biological processes linked to intra-amniotic infection/inflammation-induced IMP dehydrogenase preterm birth. “
“National Institute for Medical Research, London, UK Cancer Research UK London Research Institute, London, UK The early growth response (Egr) transcription factor family regulates multiple steps during T-cell development. We examine here the role played by Egr2 in positive selection. In double-positive cells, Egr2 is upregulated immediately following TCR ligation, and its expression requires both the MAPK and calcineurin signaling pathways. Inducible transgenic and knockout mice were generated to cause gain- or loss-of-function of Egr2 in double-positive cells, and had reciprocal effects; more mature single-positive cells were made when Egr2 was overexpressed, and fewer when Egr2 was absent. These defects were associated with changes in the survival of positively selected cells rather than perturbation of positive selection or immediate post-selection signaling.

17,18 Itraconazole.  Itraconazole is marketed as a capsule containing itraconazole-coated sugar pellets, and solubilised in hydroxypropyl-β-cyclodextrin (HP-βCD) for oral and i.v. use. The i.v. solution is no longer available in the United States. While there is no evidence to date that HP-βCD contributes to the drug interaction potential of itraconazole, it does impact the extent of absorption of oral itraconazole. Itraconazole exhibits dose-dependent (nonlinear) pharmacokinetics,

and its rate and extent of absorption differ depending on its oral formulation. Absorption from the capsule is variable, slow, incomplete and optimal in an acidic gastric environment or in the fed state.19 beta-catenin cancer In contrast, because itraconazole is solubilised in HP-βCD in the oral solution, it requires no dissolution,

and thus its absorption is rapid and unaffected by changes in gastric pH.20 As the itraconazole capsule must first undergo dissolution, the concentration that goes into solution in gastric fluid naturally varies depending on gastric pH and gastric emptying. Therefore, the amount delivered to the intestinal epithelium may be insufficient to saturate intestinal CYP3A4, and thus the capsule undergoes significant presystemic (‘first-pass’) metabolism in the intestine in addition to the liver before reaching the systemic circulation.21,22 In contrast, the oral solution delivers high itraconazole concentrations to the intestinal epithelium that may transiently saturate intestinal Selleckchem JNK inhibitor CYP3A4 and thereby somewhat minimise presystemic metabolism

by intestinal CYP3A4.21,22 Thus, the solution produces higher and less variable serum itraconazole concentrations of than the capsule.23 The solution produces higher Cmax plasma itraconazole concentrations when ingested in the fasted state compared with non-fasting conditions.21,22 However, even in the fed state, the solution produces higher serum concentrations than the capsule.21,22 Itraconazole binds extensively (99.8%) to albumin, and thus the unbound itraconazole concentrations in body fluids (i.e. CSF, saliva, urine) are very low.24 This azole distributes widely throughout the body, has high affinity for tissues (i.e. vaginal mucosa, horny layer of nails, etc.) and can persist in these tissues long after the serum concentrations are undetectable.24 Itraconazole is highly lipophilic and undergoes extensive biotransformation in humans. Approximately 2% of an itraconazole dose is excreted unchanged in the urine.19,24 The biotransformation involves stereoselective sequential metabolism catalysed by CYP3A4.25–27 To date, only three (hydroxy-itraconazole, keto-itraconazole and N-desalkyl-itraconazole) of the many theorised itraconazole metabolites have been identified.25–27 All three metabolites are formed only by CYP3A4.25 Current itraconazole formulations contain a mixture of four stereoisomers.

Furthermore, AnnexinV stainings of splenic B cells one day after setting up the in vitro cultures revealed that in contrast to pre-B cells, B cells did not respond to overexpression of Pim1 by increased survival (Fig. 5E). We conclude that overexpression of Pim1 and Myc does not induce ex vivo isolated splenic or peritoneal CD19+ sIgM+ immature or mature B cells to long-term polyclonal proliferation, or selective survival and extended proliferation in the

absence or presence of polyclonal B-cell stimulators. Our experiments presented in this paper describe the effect of the inducible Pexidartinib research buy single or double overexpression of the proto-oncogenes Pim1 and Myc in mouse B-lymphocytes at different stages of development, starting at the DJH/DJH-rearranged pre-BI cell stage 1. Many experiments studying the effect of proto-oncogenes on hematopoietic cells have been done using transgenic mice, also in the case of Pim1 and Myc 18. These mice express the transgenes under the control of the μ enhancer of the immunoglobulin heavy chain (Eμ), which is expressed already at a very early stage of B-cell development. The limitation of such transgenic mice is that if the team play

of the transgenic proto-oncogenes leads to a block in differentiation at an early stage of cell differentiation (as it is the case in these Eμ Pim1/Myc transgenic mice), it is not possible to study effects of the proto-oncogenes on later differentiation stages of the cells using these mice. To circumvent this, we used MI-503 purchase an inducible system to overexpress the two proto-oncogenes, which allowed us to evaluate the effect of proto-oncogene overexpression at different stages of maturation. In the experiments presented here, we have used retroviral vectors to overexpress the proto-oncogenes in B-lymphocytes under the control of a doxycycline-inducible promoter. Retroviral vectors are known to induce transformations by themselves by activating surrounding host genes with their LTR promoters and enhancers. Hence,

we used self-inactivating vectors. It can be expected that three subsequent transductions, performed with the pre-BI cells, have generated a genetically heterogenous collection of transduced cells with differential inducibility of Pim1 and Myc. As one example, such transgenetic heterogeneity might well be the reason why only a fraction of the Pim1/Myc-double-transduced PD184352 (CI-1040) pre-BI cells initiate proliferation upon proto-oncogene induction, probably either due to inactivation of a transgene or inappropriate overexpression levels of the transgene(s). In spite of these disadvantages, the results of our experiments show that retroviral vectors allow the rapid testing of different combinations of proto-oncogenes in our pre-BI cell lines and their differentiated descendants. Our cell cycle analyses with the Myc-single- and the Pim1/Myc-double-overexpressing pre-B cells show an increase of the frequency of cells in cell cycle.

Treg frequencies were increased in second and third trimester in LMWH-treated thrombophilic pregnancies compared to controls. Treg levels were comparable to those of normal pregnancies. Homozygous FVL mice had decreased decidual Tregs compared to wild-type mice. LMWH treatment normalized Tregs and was associated with increased decidual IL-10 mRNA. LMWH diminished Caspase-3-activity in mice of all genotypes. We demonstrated anti-apoptotic and anti-inflammatory effects of LMWH in pregnant FVL mice. LMWH increased see more Treg levels

in mice and humans, which suggests benefits of LMWH treatment for thrombophilic women during pregnancy. “
“Disruption of the interaction of bromo and extraterminal (BET) proteins with acetylated histones using small molecule inhibitors

suppresses Myc-driven cancers and TLR-induced inflammation in mouse models. The predominant mechanism of BET inhibitor action is to suppress BET-mediated recruitment of positive transcription elongation factor b and, thus, transcription elongation. We investigated the effects of BET inhibitor I-BET151 on transcriptional responses to TLR4 and TNF in primary human monocytes and also on responses to cytokines IFN-β, IFN-γ, IL-4, and IL-10, which activate the JAK-STAT signaling pathway and are important for monocyte polarization and inflammatory diseases. I-BET151 suppressed TLR4- and TNF-induced IFN responses by diminishing both autocrine IFN-β expression and transcriptional responses to IFN-β. I-BET151 inhibited Gefitinib cytokine-induced transcription of STAT targets in a gene-specific manner without affecting High Content Screening STAT activation or recruitment. This inhibition was

independent of Myc or other upstream activators. IFN-stimulated gene transcription is regulated primarily at the level of transcription initiation. Accordingly, we found that I-BET151 suppressed the recruitment of transcriptional machinery to the CXCL10 promoter and an upstream enhancer. Our findings suggest that BET inhibition reduces inflammation partially through suppressing cytokine activity and expands the understanding of the inhibitory and potentially selective immunosuppressive effects of inhibiting BET proteins. “
“A growing body of evidence points to autophagy as an essential component in the immune response to tuberculosis. Autophagy is a direct mechanism of killing intracellular Mycobacterium tuberculosis and also acts as a modulator of proinflammatory cytokine secretion. In addition, autophagy plays a key role in antigen processing and presentation. Autophagy is modulated by cytokines; it is stimulated by T helper type 1 (Th1) cytokines such as tumour necrosis factor (TNF)-α and interferon (IFN)-γ, and is inhibited by the Th2 cytokines interleukin (IL)-4 and IL-13 and the anti-inflammatory cytokine IL-10.

Immunization with peptides together with adjuvants such as CFA, LPS, or CpG, is able to induce small populations of memory CD8+ T cells. Unfortunately, these populations accumulate primarily in the local draining LN (dLN) and are largely undetectable by direct ex vivo assays, requiring in vitro secondary expansion for detection 10–13. Recent studies have reported some success at improving these apparent limitations and describe the induction of memory T-cell populations using synthetic peptide antigens 14–19. However, these studies have employed repeated immunizations, high

doses of antigen, large quantities of recombinant cytokines, and/or potent agonistic antibodies selleck chemical to T-cell costimulatory machinery – strategies that may not be feasible in a mass vaccination setting. Here we describe studies aimed to characterize the basic features of the CD8+ T-cell responses induced by immunization with short synthetic peptides. We tracked GS-1101 cost the response of TCR-Tg T cells to a vaccination of peptide alone and in combination with different TLR agonists and found that soluble peptides alone are highly immunogenic in vivo, but fail to induce mechanisms promoting the survival of activated T cells. Indeed, peptide-primed CD8+ T cells display unique phenotypic features indicative

of poor survival and inability to expand. Further, we identify the TLR-9 agonist, CpG, and B cells as major factors that can

positively and negatively affect, respectively, the establishment of long-term memory CD8+ T-cell populations in response to peptide immunization. To study the CD8+ T-cell responses to soluble peptide immunization, we used an experimental system based on the adoptive transfer of naïve CD8+ T cells expressing a TCR-Tg specific for the epitope SYVPSAEQI from the CS protein of P. yoelii malaria parasites. Given that primary T-cell responses to peptide-based immunization have Arachidonate 15-lipoxygenase been difficult to detect directly ex vivo or upon transfer of small numbers 2×103 TCR-Tg cells (Supporting Information Fig. 1), we began our studies by transferring 5×105 CFSE-labeled TCR-Tg T cells so that early priming events could be readily visualized by the dilution profile of the labeled T cells. We established that as little as 2.5 μg of peptide in PBS induced a strong proliferative response, detectable as early as 3 days after immunization in the spleen and in the LN draining the site of immunization (Fig. 1A). In fact, as little as 0.25 μg of peptide was able to induce measurable T-cell proliferation in the LN draining the site of immunization, though a systemic response was not observed. Increasing the amount of peptide to 25 μg resulted in an unphysiological T-cell proliferation profile. Thus, we carried out further experiments with a peptide dose range of 2.5–5 μg.

RIG-I, LGP2, and their adaptor IPS-1 are conserved in the lamprey genome, while MDA5 is not found. Interestingly, although NF-κB and its activating genes, such as TBK1 and IKKε, are highly conserved among vertebrates, IRF3, IRF7, type I IFN and inflammatory cytokine genes, such as IL-12p40, IL-6 PLK inhibitor and TNFα, have not been found in the lamprey genome. These observations imply that the TLR and RLR pathways are incomplete in jawless vertebrates. Because IL-12 and type I IFN play important roles in direct or indirect activation and differentiation of T cell subsets in jawed vertebrates, their absence in jawless vertebrates implies that the molecular

basis of the innate immune system in jawless vertebrates is distinct from that of jawed vertebrates (5b) [57], [58]. In mammals, the TLR and RLR pathways play a critical role in activation of T and B adaptive immune cells [53]. For AZD1152-HQPA research buy example, dsRNA such as poly I:C acts as an adjuvant, enhancing adaptive immune responses through the TLR3/TICAM-1 and MDA5/IPS-1 pathways. In TICAM-1 and IPS-1 deficient mice, both antigen-specific antibody production and CD8+ T cell expansion are decreased after poly I:C stimulation [59]. Previous studies have also shown that antigen-specific antibody production in jawless vertebrates is effectively induced against microbes containing PAMPs, which act as adjuvants, in comparison with purified protein antigens

[14]. Hence, as in jawed vertebrates, initiation of adaptive immune responses in jawless vertebrates appears to require prior activation of the innate immune system. Recently, myeloid cells that resemble DCs in mammals have been identified in teleost fish [60], [61]. Activation of these DC-like cells by stimulation with TLR ligands induces expression of IL-12p40 and maturation marker CD83 similarly to mammalian DCs. Moreover, DC-like cells are not only highly phagocytic of foreign antigens such as bacteria but also enhance proliferation of antigen-specific

T cells. Previous studies in jawless vertebrates have shown that polymorphonuclear myeloid cells phagocytose mammalian erythrocytes [62]. Additionally, the TLR3 and TLR5 genes, which are expressed in mammalian DCs and teleost Calpain DC-like cells, are expressed in VLRA−/VLRB− cells [27]. These observations indicate that VLRA−/VLRB− myeloid cells, which phagocytose foreign antigens, may function as accessory cells that activate the VLR-based adaptive immune system. Although the molecular details of the innate and adaptive immune systems differ between jawless and jawed vertebrates, both immune systems are similar in jawless vertebrates and jawed vertebrates. The functions of VLRA+ and VLRC+ LLCs and the mechanisms of self-tolerance in thymoids are still unknown. Additionally, the molecular and cellular basis for crosstalk between the innate and adaptive immune systems in jawless vertebrates is also unclear.

However, in vivo phagocytosis may be accomplished in the LO. LO has been proposed as the principal tissue for the removal of foreign material from the hemolymph. Foreign material present in the hemolymph is agglutinated, phagocyted and degraded in LO. Engulfed material is then destroyed in the LOS (7,8). The LO is invaded by hemocytes, and it has been suggested that this invasion is responsible for the immune related activities within the LO (9). Although the identification of crustacean hemocytes is essential to elucidate their specific immune reactions (10), characterization of hemocyte subpopulations remains uncertain. On the basis of their morphology and presence

of granules, hemocytes are usually classified into three subpopulations; LGH, SGH, and HH (10,11). However, different criteria exist about the nature of HH. According to Hose et al. (12) and Gargioni selleck compound and Barraco (10), HH constitute a differentiated cell subpopulation, characterized by the presence of cytoplasmic glycoprotein deposits and striated granules. Other authors consider HH as undifferentiated hemocytes, precursors of SGH (13) or LGH and SGH (14). Rodríguez et al. (15) identified three monoclonal antibodies (MABs), which could be used as hemocyte subpopulation markers. Antigenic

characterization of shrimp hemocytes separated by isopycnic centrifugation on a discontinuous percoll gradient, showed that 40E2 MAB exhibited specific labeling of LGH, 40E10 MAB recognized vesicles present in SGH and 41B12 MAB labeled vesicles NVP-LDE225 in vivo of hyaline hemocytes (16,17). By western blot and ELISA, Astemizole the MAB 41B12 recognized α2-macroglobulin of crayfish, human, and Farfantepenaeus paulensis (15,17,18). Interestingly Perazzolo et al. (18) reported cellular localization of α2-macroglobulin in granules of LGH. Hemocytes subpopulations involved in the clearance process at the LO require

further studies. Based on PO activity assays, several authors reported the presence of SGH and LGH in the LO and LOS. In addition, van de Braak et al. (19) and Shao et al. (20) reported by ultrastructure the presence of SGH-like cells in the LO. Shao et al. (20) considered the presence of SGH in LO during the infection process to be due to light PO activity in the stromal matrix of LO. Anggraeny and Owens (21) observed low PO activity solely in the LOS and indicated that spent LGH and SGH form spheroids. Winotaphan et al. (22) and van de Braak et al. (23), restrict the presence of HH in the LO to being precursors of granular hemocyte, indicating that LO can be a place of hemocyte differentiation. In this study we used MABs 41B12, 40E10 and 40E2 in order to better understand the role of hemocyte subpopulations involved in the immune process occurring in the LO of L. vannamei.